gmk_gs vicinity.txt

GSE10010_series_matrix.txtimp_info.txt
IL-22 r is 2 
Found -/- in !Series_summary	"Infection by attaching and effacing (A/E) pathogens poses a serious threat to public health, as was highlighted by the recent outbreak of E. coli O157:H7 infection in the United States. Here, by using a murine A/E pathogen, Citrobacter rodentium, we demonstrate that C. rodentium infection is lethal to IL-22-/- mice within two weeks. IL-22, in the early phase of infection, is indispensable for preventing the invasion of bacteria through the intestinal epithelium, and thereby preventing systemic spread and mortality.  We also show that IL-23 is required for the early induction of IL-22 during C. rodentium infection. Finally, our data suggest that IL-22 exerts its function by boosting the innate immune responses of colonic epithelial cells, especially though the induction of anti-microbial proteins, RegIIIβ and RegIIIγ."
GSE10010_series_matrix.txtimp_info.txt
IL-23 r is 2 
Found -/- in !Series_summary	"Infection by attaching and effacing (A/E) pathogens poses a serious threat to public health, as was highlighted by the recent outbreak of E. coli O157:H7 infection in the United States. Here, by using a murine A/E pathogen, Citrobacter rodentium, we demonstrate that C. rodentium infection is lethal to IL-22-/- mice within two weeks. IL-22, in the early phase of infection, is indispensable for preventing the invasion of bacteria through the intestinal epithelium, and thereby preventing systemic spread and mortality.  We also show that IL-23 is required for the early induction of IL-22 during C. rodentium infection. Finally, our data suggest that IL-22 exerts its function by boosting the innate immune responses of colonic epithelial cells, especially though the induction of anti-microbial proteins, RegIIIβ and RegIIIγ."
GSE10010_series_matrix.txtimp_info.txt
IL-22 r is 2 
Found treated in !Series_overall_design	"Control or IL-22-treated mouse colon in triplicate."
GSE10029-GPL6328_series_matrix.txtimp_info.txt
PBE r is 1 
Found treated in !Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."
GSE10029-GPL6328_series_matrix.txtimp_info.txt
GTPase r is 8 
Found induced in !Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6328_series_matrix.txtimp_info.txt
Rho r is 7 
Found induced in !Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6328_series_matrix.txtimp_info.txt
Vav2 r is 5 
Found induced in !Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6329_series_matrix.txtimp_info.txt
PBE r is 1 
Found treated in !Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."
GSE10029-GPL6329_series_matrix.txtimp_info.txt
GTPase r is 8 
Found induced in !Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6329_series_matrix.txtimp_info.txt
Rho r is 7 
Found induced in !Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6329_series_matrix.txtimp_info.txt
Vav2 r is 5 
Found induced in !Series_summary	"Tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6330_series_matrix.txtimp_info.txt
PBE r is 1 
Found treated in !Series_overall_design	"The experiments addressed the effect of TNF exposure.  8-12-week-old NOD.BDC2.5 transgenic mice were injected i.p. with PBS or 3 ug murine TNFalpha; on alternate days for three weeks.  At day 24 of treatment, suspensions of LNs and/or splenocytes were stimulated with the indicated concentration of the mimotope (1047-7 peptide (YVAPVWVRME)) at a density of 7-8 x 106 cells/ml, in a final volume of 1 ml in 24-well plates.  After prolonged in vitro culture, cells were harvested 12 hrs post transplantation.  CD4+ T cells were purified by labeling of monoclonal Abs of surface markers, Vbeta4-FITC and CD4-PE and enriched by Magnetic beads selection followed by FACS sorting.  The purity of CD4+ T cells ranged from 95% to 99% depending on individual CD4 T cells preparation.  The data in column represents six independent repeated experiments with half of the slides being reverse replicates.  We compared RNA from PBE treated group with TNF treated group without including reference RNA."
GSE10029-GPL6330_series_matrix.txtimp_info.txt
GTPase r is 8 
Found induced in !Series_summary	"tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6330_series_matrix.txtimp_info.txt
Rho r is 7 
Found induced in !Series_summary	"tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10029-GPL6330_series_matrix.txtimp_info.txt
Vav2 r is 5 
Found induced in !Series_summary	"tumor necrosis factor alpha (TNFalpha) plays an important role in immune regulation, inflammation, and autoimmunity.  Chronic TNFalpha exposure has been shown to down-modulate T cell responses.  In a mouse T cell hybridoma model, TNFalpha attenuated T cell receptor (TCR) signaling.  We have confirmed that chronic TNFalpha and anti-TNFalpha exposure suppressed and increased T cell responses in BDC2.5 CD4+ T cells, respectively.  The goal of this study is to analyze global transcriptional alterations resulting from TNFalpha treatment on TCR signaling pathways using cDNA microarrays.  We found that genes involved in functional categories including T cell signaling, cell cycle, proliferation, ubiquitination, cytokine synthesis, calcium signaling, and apoptosis were modulated.  Genes such as ubiquitin family genes, cytokine inducible SH2-containing genes, cyclin-dependent kinase inhibitors p21, p57, calmodulin family genes (calmodulin -V1, -V2, and ?V3) and calcium channel voltage- dependent, N type alpha1B subunit (CaV2.2) were induced by TNFalpha, while Vav2, Rho GTPase activating protein, calcium channel voltage dependent, L type alpha 1C subunit (CaV1.2), interleukin-1 (IL) receptor-associated kinase 1, and -V2 (IRAK-1and -2) and IL enhancer binding factor 3 were reduced by TNFalpha.  Genes such as CaV1.2 and proliferating cell nuclear antigen, repressed by TNFalpha, were induced by anti-TNF treatment.  Further, we showed that chronic TNFalpha exposure impaired NF-kappaB and AP-1 transactivation activity, leading to T cell unresponsiveness.  Thus, our results present a detailed picture of transcriptional programs affected by chronic TNFalpha exposure, and provide candidate target genes, which may function to mediate TNFalpha induced T cell unresponsiveness."
GSE10067_series_matrix.txtimp_info.txt
HSL r is 2 
Found knockout in !Series_title	"Gene expression data from murine liver samples comparing hormone sensitive lipase (HSL) knockout mice vs. wildtype mice"
GSE10067_series_matrix.txtimp_info.txt
lipase r is 4 
Found knockout in !Series_title	"Gene expression data from murine liver samples comparing hormone sensitive lipase (HSL) knockout mice vs. wildtype mice"
GSE10067_series_matrix.txtimp_info.txt
HSL r is 1 
Found knockout in !Series_summary	"HSL is a key enzyme in in the mobilization of fatty acids from the triglyceride stores of white adipose tissue. In addition, it is expressed in mice liver.  In the present microarray study, changes in the transcript profile of murine liver samples due to global HSL knockout were investigated."
GSE10067_series_matrix.txtimp_info.txt
HSL r is 3 
Found knockout in !Series_overall_design	"Genetic modification to analyze the impact of a general knockout of the HSL gene on liver metabolism."
GSE10067_series_matrix.txtimp_info.txt
HSL r is 1 
Found null in !Series_overall_design	"HSL knockout (ko) mice versus wildtype (wt) mice. Mice fed a normal diet (ND) versus mice fed a high fat diet (FD) for 6 months. Equal amounts of liver samples from six mice were pooled and total RNA was extracted, except for HSL-null mice on FD were only 4 livers were pooled."
GSE10082_series_matrix.txtimp_info.txt
Ahr r is 1 
Found null in !Series_summary	"Conventional biochemical and molecular techniques identified previously several genes whose expression is regulated by the aryl hydrocarbon receptor (AHR). We sought to map the complete spectrum of AHR-dependent genes in male adult liver using expression arrays to contrast mRNA profiles in Ahr-null mice (Ahr–/–) with those in mice with wild-type AHR (Ahr+/+). Transcript profiles were determined both in untreated mice and in mice treated 19 h earlier with 1000 µg/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of 456 ProbeSets was significantly altered by TCDD in an AHR-dependent manner, including members of the classic AHRE-I gene battery, such as Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1. In the absence of exogenous ligand, AHR status alone affected expression of 392 ProbeSets, suggesting that the AHR has multiple functions in normal physiology. In Ahr–/– mice, only 32 ProbeSets exhibited responses to TCDD, indicating that the AHR is required for virtually all transcriptional responses to dioxin exposure in liver. The flavin-containing monooxygenases, Fmo2 and Fmo3, considered previously to be uninducible, were highly induced by TCDD in an AHR-dependent manner. The estrogen receptor alpha as well as two estrogen-receptor-related genes (alpha and gamma) exhibit AHR-dependent expression, thereby extending cross-talk opportunities between the intensively studied AHR and estrogen receptor pathways. p53 binding sites are over-represented in genes down-regulated by TCDD, suggesting that TCDD inhibits p53 transcriptional activity. Overall, our study identifies a wide range of genes that depend on the AHR, either for constitutive expression or for response to TCDD."
GSE10134_series_matrix.txtimp_info.txt
estrogen receptor r is 2 
Found expressing in !Series_summary	"We employed a gene complementation strategy combined with microarray screening to identify miRNAs involved in the formation of erythroid (red blood) cells.  To search for GATA-1-regulated erythroid miRNAs, we used the Gata-1– erythroblast line G1E.  These cells proliferate in culture as immature erythroid precursors and undergo terminal maturation when GATA-1 activity is restored.  G1E-ER4 is a sub-line stably expressing an estrogen-activated form of GATA-1 (GATA-1 fused to the ligand binding domain of the estrogen receptor).  Treatment of G1E-ER4 cells with estradiol induces a GATA-1-regulated program of gene expression with concomitant cellular maturation.  We used a microarray to evaluate the expression of 292 different miRNAs in G1E-ER4 cells at 0 versus 24 hours after GATA-1 activation.  Affymetrix gene expression profiling has previously been deposited (GEO accession no. GSE628)."
GSE10162_series_matrix.txtimp_info.txt
Clc5 r is 3 
Found knockout in !Series_summary	"Dent disease has multiple defects attributed to proximal tubule malfunction including low molecular weight proteinuria, aminoaciduria, phosphaturia and glycosuria. In order to understand the changes in kidney function of the Clc5 transporter gene knockout mouse model of Dent disease, we examined gene expression profiles from proximal tubules of mouse kidneys."
GSE10162_series_matrix.txtimp_info.txt
Clcn5 r is 1 
Found knockout in !Series_summary	"Overall 720 genes are expressed differentially in the proximal tubules of the Dent Clcn5 knockout mouse model compared to those of control wild type mice. The fingerprint of these gene changes may help us to understand the phenotype of Dent disease."
GSE10162_series_matrix.txtimp_info.txt
Clcn5 r is 4 
Found knockout in !Series_summary	"Keywords: gene knockout, mouse, Clcn5, Dent's disease"
GSE10162_series_matrix.txtimp_info.txt
Clcn5 r is 1 
Found knockout in !Series_overall_design	"Renal proximal tubules were dissected from wild type and Clcn5 knockout mice. Mice were anesthetized with halothane, the abdominal aorta of each animal was accessed and the left kidney was perfused with an ice-cold salt.  Proximal tubule dissection was performed in an ice-cold salt solution. After dissection of approximately 80-100 segments of 2 mm in length per kidney, the RNA for 3-4 mice was combined to have enough RNA per chip."
GSE10166_series_matrix.txtimp_info.txt
aryl hydrocarbon receptor r is 3 
Found activation in !Series_summary	"Over-activation of the aryl hydrocarbon receptor by TCDD in mice leads among other phenotypes to a severe thymic atrophy accompanied by immunosuppression. TCDD causes a block in thymocyte maturation and a preferential emigration of immature CD4-CD8- DN thymocytes (recent thymic emigrants) into the periphery. As part of this study gene expression profiles from DN thymocytes and thymic emigrants were generated from TCDD and solvent control mice"
GSE10167_series_matrix.txtimp_info.txt
Tcof1 r is 1 
Found haploin-sufficiency in !Series_summary	"The object of this study was to identify genes transcriptionally upregulated and downregulated in response to Tcof1 haploin-sufficiency during mouse embryogensis"
GSE10168_series_matrix.txtimp_info.txt
ET r is 5 
Found activation in !Series_title	"AhR activation by TCDD in the ET, cortical epithelial cell line"
GSE10168_series_matrix.txtimp_info.txt
aryl hydrocarbon receptor r is 3 
Found activation in !Series_summary	"Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line."
GSE10175_series_matrix.txtimp_info.txt
Tcfap2c r is 1 
Found mutant in !Series_title	"Comparison of gene expression in the epidermis of Tcfap2c mutant and control skin at embryonic day 16.5"
GSE10175_series_matrix.txtimp_info.txt
Ly6/Plaur domain containing 1 r is 6 
Found mutant in !Series_summary	"The development of the epidermis, a stratified squamous epithelium, is dependent on the regulated differentiation of keratinocytes. Differentiation begins with the initiation of stratification, a process tightly controlled through proper gene expression. AP-2γ is expressed in skin and previous research suggested a pathway where p63 gene induction results in increased expression of AP-2γ which in turn is responsible for induction of K14. This study uses a conditional gene ablation model to further explore the role of AP-2γ in skin development.  Mice deficient for AP-2γ exhibited delayed expression of p63, K14, and K1, key genes required for development and differentiation of the epidermis. In addition, microarray analysis of E16.5 skin revealed delayed expression of additional late epidermal differentiation genes: filaggrin, repetin and secreted Ly6/Plaur domain containing 1, in mutant mice. The genetic delay in skin development was further confirmed by a functional delay in the formation of an epidermal barrier. These results document an important role for AP-2γ in skin development, and reveal the existence of regulatory factors that can compensate for AP-2γ in its absence."
GSE10175_series_matrix.txtimp_info.txt
secreted Ly6/Plaur domain containing 1 r is 7 
Found mutant in !Series_summary	"The development of the epidermis, a stratified squamous epithelium, is dependent on the regulated differentiation of keratinocytes. Differentiation begins with the initiation of stratification, a process tightly controlled through proper gene expression. AP-2γ is expressed in skin and previous research suggested a pathway where p63 gene induction results in increased expression of AP-2γ which in turn is responsible for induction of K14. This study uses a conditional gene ablation model to further explore the role of AP-2γ in skin development.  Mice deficient for AP-2γ exhibited delayed expression of p63, K14, and K1, key genes required for development and differentiation of the epidermis. In addition, microarray analysis of E16.5 skin revealed delayed expression of additional late epidermal differentiation genes: filaggrin, repetin and secreted Ly6/Plaur domain containing 1, in mutant mice. The genetic delay in skin development was further confirmed by a functional delay in the formation of an epidermal barrier. These results document an important role for AP-2γ in skin development, and reveal the existence of regulatory factors that can compensate for AP-2γ in its absence."
GSE10182_series_matrix.txtimp_info.txt
Nod2 r is 2 
Found induced in !Series_summary	"The transcriptome induced via Nod2 stimulation is greatly expanded in TLR2-tolerant macrophages."
GSE10182_series_matrix.txtimp_info.txt
Nod2 r is 1 
Found stimulation in !Series_summary	"The transcriptome induced via Nod2 stimulation is greatly expanded in TLR2-tolerant macrophages."
GSE10200_series_matrix.txtimp_info.txt
MYC r is 1 
Found inactivation in !Series_summary	"Keywords: Dose response - MYC inactivation by doxycycline treatment"
GSE10210_series_matrix.txtimp_info.txt
VE-cadherin r is 1 
Found expressing in !Series_title	"Gene expression analysis of embryonic stem cells expressing VE-cadherin (CD144) during endothelial differentiation"
GSE10210_series_matrix.txtimp_info.txt
VE-cadherin r is 7 
Found expressing in !Series_summary	"Endothelial differentiation occurs during normal vascular development in the developing embryo. Mouse embryonic stem (ES) cells were used to further define the molecular mechanisms of endothelial differentiation. By flow cytometry a population of VEGF-R2 positive cells was identified as early as 2.5 days after differentiation of ES cells, and a subset of VEGF-R2 + cells, that were CD41+ positive at 3.5 days.  A separate population of VEGF-R2+ stem cells expressing the endothelial-specific marker CD144 (VE-cadherin) was also identified at this same time point. Microarray analysis of >45,000 transcripts was performed on RNA obtained from cells expressing VEGF-R2, CD41, and CD144."
GSE10210_series_matrix.txtimp_info.txt
CD41 r is 8 
Found expressing in !Series_overall_design	"We identified four populations of cells; cells expressing VEGF-R2 (day 2.5), CD41 expressing cells (day 3.5), cells expressing CD144 (VE-Cadherin, day 3.5), and cells expressing CD144 (day 6.5). In addition to this, we have also obtained the negative control cells at each time such as VEGF-R2 (day 2.5) negative, CD41 negative (day 3.5), CD144 negative (VE-Cadherin, day 3.5), and negative CD144 (day 6.5). RNA for the microarray experiments were obtained in duplicate from two separately conducted experiments using the murine embryonic stem cells.."
GSE10210_series_matrix.txtimp_info.txt
R2 r is 2 
Found expressing in !Series_overall_design	"We identified four populations of cells; cells expressing VEGF-R2 (day 2.5), CD41 expressing cells (day 3.5), cells expressing CD144 (VE-Cadherin, day 3.5), and cells expressing CD144 (day 6.5). In addition to this, we have also obtained the negative control cells at each time such as VEGF-R2 (day 2.5) negative, CD41 negative (day 3.5), CD144 negative (VE-Cadherin, day 3.5), and negative CD144 (day 6.5). RNA for the microarray experiments were obtained in duplicate from two separately conducted experiments using the murine embryonic stem cells.."
GSE10216_series_matrix.txtimp_info.txt
Emx2 r is 1 
Found KO in !Series_overall_design	"The epithelial cells of the gonadal primordium were obtained by Laser Microdissection System. The specimens prepared from three individuals were mixed as one pool. There are three experimental replicates in each genotype, 3-pools of wild-type and 3-pools of Emx2 KO mouse."
GSE10218_series_matrix.txtimp_info.txt
Fos r is 1 
Found deletion in !Series_title	"Keratinocyte specific Fos-deletion in K5-Sos-F mouse tumor model"
GSE10218_series_matrix.txtimp_info.txt
K5 r is 2 
Found deletion in !Series_title	"Keratinocyte specific Fos-deletion in K5-Sos-F mouse tumor model"
GSE10218_series_matrix.txtimp_info.txt
Fos r is 1 
Found deletion in !Series_summary	"Keywords: Fos-deletion, Fos-floxed, K5-SOS-F mouse tumor model, skin papilloma, global gene expression, microarray, Fos target in skin carcinogenesis"
GSE10218_series_matrix.txtimp_info.txt
K5 r is 5 
Found deletion in !Series_summary	"Keywords: Fos-deletion, Fos-floxed, K5-SOS-F mouse tumor model, skin papilloma, global gene expression, microarray, Fos target in skin carcinogenesis"
GSE10218_series_matrix.txtimp_info.txt
Fos r is 1 
Found deletion in !Series_overall_design	"In the present Experiment two different genotypes in combination with an established mouse tumor model were compared. An active form of the Sos (son of sevenless) is expressed under a keratin5 promoter leading to a constitutive activation of the Ras-Raf pathway, which results in skin papilloma formation. In the context of this tumor model an epidermis specific homozygote Fos-deletion was compared to homozygous floxed Fos-alleles. Both genotypes (Fos-deleted and Fos-floxed) were treated equally. The specimens were taken from skin papilloma at the mouse tail. A total number of six specimens from six different individuals (three biological replicates per genotype) were taken. Each sample was prepared and hybridized against Universal Mouse Reference RNA (Stratagene) in a dye-swap experiment, resulting in two technical replicates for each specimen, respectively."
GSE10218_series_matrix.txtimp_info.txt
Raf r is 4 
Found activation in !Series_overall_design	"In the present Experiment two different genotypes in combination with an established mouse tumor model were compared. An active form of the Sos (son of sevenless) is expressed under a keratin5 promoter leading to a constitutive activation of the Ras-Raf pathway, which results in skin papilloma formation. In the context of this tumor model an epidermis specific homozygote Fos-deletion was compared to homozygous floxed Fos-alleles. Both genotypes (Fos-deleted and Fos-floxed) were treated equally. The specimens were taken from skin papilloma at the mouse tail. A total number of six specimens from six different individuals (three biological replicates per genotype) were taken. Each sample was prepared and hybridized against Universal Mouse Reference RNA (Stratagene) in a dye-swap experiment, resulting in two technical replicates for each specimen, respectively."
GSE10235_series_matrix.txtimp_info.txt
NF r is 3 
Found inhibition in !Series_title	"Transgenic inhibition of astroglial NF-kappaB in experimental autoimmune encephalomyelitis"
GSE10235_series_matrix.txtimp_info.txt
NF-kappaB r is 3 
Found inhibition in !Series_title	"Transgenic inhibition of astroglial NF-kappaB in experimental autoimmune encephalomyelitis"
GSE10250_series_matrix.txtimp_info.txt
estrogen receptor r is 7 
Found expressing in !Series_overall_design	"Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs. In this analysis, RNA isolated from 64hr and 72hr post Ad-Cre infection were used. We extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein). In this analysis, two different MEF preparations (repl1 and repl2), two different time points (64hr and 72hr) were used for array analysis with tamoxifen-treated MEFs. For vehicle (ethanol) treated MEFs, two different MEF preparations (repl1 and repl2), and a single timepoint (64hr) was used."
GSE10273_series_matrix.txtimp_info.txt
IRF-4 r is 5 
Found lacking in !Series_summary	"Productive rearrangement of the immunoglobulin heavy chain locus triggers a major developmental checkpoint that promotes limited clonal expansion of pre-B cells, culminating in cell cycle  arrest and rearrangement of the kappa (κ) or lambda (λ) light-chain loci. B lineage cells lacking the related transcription factors IRF-4 and IRF-8 undergo a developmental arrest at the cycling pre-B cell stage and are blocked for light-chain recombination. Using Irf-4,8-/- pre-B cells we demonstrate that two pathways converge to synergistically drive light-chain rearrangement, a process that is not simply activated by cell cycle exit. One pathway is directly dependent on IRF-4, whose expression is elevated by pre-BCR signaling.  IRF-4 targets the κ 3′ and λ enhancers to increase locus accessibility and positions a kappa allele away from pericentromeric heterochromatin. The other pathway is triggered by attenuation of IL-7 signaling and results in activation of the κ intronic enhancer via binding of the transcription factor, E2A. Intriguingly, IRF-4 regulates the expression of CXCR4 and promotes the migration of pre-B cells in response to the chemokine CXCL12. We propose that IRF-4 coordinates the two pathways regulating light-chain recombination by positioning pre-B cells away from IL-7 expressing stromal cells."
GSE10273_series_matrix.txtimp_info.txt
IRF-8 r is 5 
Found lacking in !Series_summary	"Productive rearrangement of the immunoglobulin heavy chain locus triggers a major developmental checkpoint that promotes limited clonal expansion of pre-B cells, culminating in cell cycle  arrest and rearrangement of the kappa (κ) or lambda (λ) light-chain loci. B lineage cells lacking the related transcription factors IRF-4 and IRF-8 undergo a developmental arrest at the cycling pre-B cell stage and are blocked for light-chain recombination. Using Irf-4,8-/- pre-B cells we demonstrate that two pathways converge to synergistically drive light-chain rearrangement, a process that is not simply activated by cell cycle exit. One pathway is directly dependent on IRF-4, whose expression is elevated by pre-BCR signaling.  IRF-4 targets the κ 3′ and λ enhancers to increase locus accessibility and positions a kappa allele away from pericentromeric heterochromatin. The other pathway is triggered by attenuation of IL-7 signaling and results in activation of the κ intronic enhancer via binding of the transcription factor, E2A. Intriguingly, IRF-4 regulates the expression of CXCR4 and promotes the migration of pre-B cells in response to the chemokine CXCL12. We propose that IRF-4 coordinates the two pathways regulating light-chain recombination by positioning pre-B cells away from IL-7 expressing stromal cells."
GSE10290_series_matrix.txtimp_info.txt
Id4 r is 7 
Found induced in !Series_summary	"Beyond demonstrating a critical role for progesterone receptor signaling in normal mammary epithelial proliferation, the progesterone receptor knockout mouse disclosed the progesterone receptor along with its effector pathways as key determinants of mammary neoplastic progression.  Despite these advances, however, further progress in our mechanistic understanding of progesterone’s involvement in mammary morphogenesis and tumorigenesis is contingent upon defining the essential effector pathways responsible for transducing the progesterone signal into a mammary proliferative and/or pro-survival response.  Toward this goal, a judiciously chosen acute progesterone treatment regimen together with microarray methods was applied to the mammary gland of the normal mouse to uncover new effectors that operate immediately downstream of the progesterone mammary signal.  Examination of the resultant progesterone-responsive transcriptome disclosed “inhibitor of differentiation or DNA binding 4” (Id4) as a molecular target acutely induced by progesterone in the murine mammary epithelium."
GSE10291_series_matrix.txtimp_info.txt
Rho r is 3 
Found treated in !Series_summary	"To gain insights into the molecular mechanisms of oligodendrocyte differentiation, we performed microarray expression profiling of the oligodendroglial cell line, Oli-neu, treated with the Rho kinase (ROCK) inhibitor, Y-27632 or with conditioned neuronal medium. This resulted in the identification of the transmembrane protein 10 (Tmem10/Opalin), a novel type I transmembrane protein enriched in differentiating oligodendrocytes. In primary cultures, Tmem10 was abundantly expressed in O4-positive oligodendrocytes, but not in oligodendroglial precursor cells, astrocytes, microglia or neurons. In mature oligodendrocytes Tmem10 was enriched in the rims and processes of the cells and was only found to a lesser extent in the membrane sheets."
GSE10318_series_matrix.txtimp_info.txt
Tbx3 r is 2 
Found activation in !Series_overall_design	"Nppa-Cre4 (Cre4) mice were crossed with CT mice to obtain efficient activation of Tbx3 in atria of double transgenic Cre4-CT mice, as previously described (Hoogaars et al., 2007). To investigate the gene expression profile of atria of Cre4-CT mice, we performed whole genome microarray analysis using Sentrix Mouse-6 oligonucleotide beadchips."
GSE10318_series_matrix.txtimp_info.txt
Tbx3 r is 1 
Found expressing in !Series_summary	"Methods and Results: We analyzed mice ectopically expressing Tbx3 in the atrial myocardium by genome-wide microarray and expression analysis. We found a prominent role for Tbx3 in defining the nodal phenotype by repressing working myocardial genes (sarcomeric, mitochondrial, fast conduction) and cell proliferation regulators, and in inducing node-associated genes. Moreover, there was a striking induction of genes associated with endocardial cushions and mesenchyme. Using gain-of-function models, we found that in the developing heart both Tbx2 and Tbx3 induce ectopic Bmp2 and Tgfb2 expression and endocardial cushion formation. Analysis of compound Tbx2/Tbx3 mutant embryos revealed that upon loss of more than two functional alleles, expansion of the AV myocardium does not occur and AV cushions fail to form."
GSE10341_series_matrix.txtimp_info.txt
Th r is 4 
Found deficient in !Series_summary	"The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown.  When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at E13.5-E14.5, they resemble wild type fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage and edema. At E12.5, prior to the appearance of morphological deficits associated with Th deletion, catecholamine-deficient fetuses are preferentially killed by experimentally-induced hypoxia and have lower tissue pO2 than wild type siblings.  Catecholamine-deficient fetuses also induced HIF-1 target genes to a greater extent than wild type siblings, supporting the notion that null fetuses experience greater hypoxia or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby, improving oxygen delivery in wild type mice. Surprisingly, increasing maternal oxygen (FiO2 33% or 63%) prevents the effects of catecholamine-deficiency, restoring heart rate, myocardial mass and survival of Th null fetuses.  We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis as vulnerability to constitutive hypoxia increases as fetal growth accelerates during normal development."
GSE10341_series_matrix.txtimp_info.txt
Th r is 4 
Found deficient in !Series_summary	"The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown.  When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at E13.5-E14.5, they resemble wild type fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage and edema. At E12.5, prior to the appearance of morphological deficits associated with Th deletion, catecholamine-deficient fetuses are preferentially killed by experimentally-induced hypoxia and have lower tissue pO2 than wild type siblings.  Catecholamine-deficient fetuses also induced HIF-1 target genes to a greater extent than wild type siblings, supporting the notion that null fetuses experience greater hypoxia or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby, improving oxygen delivery in wild type mice. Surprisingly, increasing maternal oxygen (FiO2 33% or 63%) prevents the effects of catecholamine-deficiency, restoring heart rate, myocardial mass and survival of Th null fetuses.  We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis as vulnerability to constitutive hypoxia increases as fetal growth accelerates during normal development."
GSE10341_series_matrix.txtimp_info.txt
Th r is 1 
Found -/- in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
Th r is 1 
Found -/- in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
tyrosine hydroxylase r is 5 
Found -/- in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
Th r is 2 
Found null in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
Th r is 2 
Found null in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
tyrosine hydroxylase r is 2 
Found null in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
tyrosine hydroxylase r is 2 
Found null in !Series_overall_design	"The second aim compared wild type and tyrosine hydroxylase null E12.5 fetuses from dam exposed to hypoxia (8% oxygen) for 6 hours prior to sacrifice at E12.5 of gestation. This resulted in 6 arrays."
GSE10386_series_matrix.txtimp_info.txt
RIP140 r is 1 
Found knockout in !Series_overall_design	"for macrophages from RIP140 knockout or wild-type mice. "
GSE10403_series_matrix.txtimp_info.txt
granzyme B r is 4 
Found expressing in !Series_summary	"IL-2 and IL-21 are closely related cytokines that might have arisen by gene duplication. Both cytokines promote the function of effector CD8+ T cells, but their distinct effects on antigen-driven differentiation of naïve CD8+ T cells into effector CD8+ T cells are not clearly understood. We found that antigen-induced expression of eomesodermin and maturation of naïve CD8+ T cells into granzyme B and CD44 expressing effector CD8+ T cells was enhanced by IL-2, but, unexpectedly, suppressed by IL-21. Furthermore, IL-21 repressed expression of IL-2Ra and inhibited IL-2-mediated acquisition of a cytolytic CD8+ T cell phenotype. Despite its inhibitory effects, IL-21 did not induce anergy, but instead potently enhanced the capacity of cells to mediate tumor regression upon adoptive transfer. In contrast, IL-2, surprisingly, impaired the subsequent anti-tumor function of transferred cells. Gene expression studies revealed a distinct IL-21-program that was characterized phenotypically by increased expression of L-selectin and functionally by enhanced anti-tumor immunity that was not reversed by secondary in vitro stimulation with antigen and IL-2. Thus, the efficacy of CD8+ T cells for adoptive immunotherapy can be influenced by opposing differentiation programs conferred by IL-2 and IL-21, a finding with important implications for the development of cellular cancer therapies."
GSE10421_series_matrix.txtimp_info.txt
Smad4 r is 3 
Found deficient in !Series_summary	"Results: Among 1419 transcripts significantly modulated by the dietary iron content, four were regulated similarly to the hepcidin genes Hamp1 and Hamp2. They are coding for Bmp6, the regulator of Bmp/Smad signal transduction Smad7, the negative regulator of basic helix-loop-helix (bHLH) proteins Id1, and a protein with a bHLH domain, Atoh8. The iron overload developed by Smad4 and Hamp1-deficient mice also increased Bmp6 transcription. Body iron stores influence Smad1/5/8 phosphorylation and, as shown by analysis of mice with liver-specific disruption of Smad4, the binding partner for the receptor-activated Smads is necessary for activation of Smad7, Id1, and Atoh8 transcription by iron."
GSE10421_series_matrix.txtimp_info.txt
hepcidin r is 6 
Found induced in !Series_summary	"Background & Aims: Although hepcidin expression was shown to be induced by the BMP signaling pathway, it is not yet known how iron regulates hepcidin and which of the BMP molecules is the endogenous regulator of iron homeostasis in vivo. We therefore assessed liver transcription profiles of mice fed an iron-deficient or an iron-enriched diet and looked for genes that were regulated similarly to hepcidin in that context."
GSE10422_series_matrix.txtimp_info.txt
Traf3 r is 3 
Found knockout in !Series_title	"Traf2 and Traf3 B cell knockout mice and Baff tg mice - gene expression in lymph node B cells"
GSE10422_series_matrix.txtimp_info.txt
Traf2 r is 3 
Found knockout in !Series_overall_design	"Lymph node B cells were purified from Traf2 B cell knockout mice, Traf3 B cell knockout mice, Baff-tg mice and respective controls.  RNA was extracted and hybridised to Affymetrix 430 2.0 Mouse Genome Arrays.  Samples were processed and hence analysed on three spearate days.  Day 1 two control mice: Traf2lox/lox pool and CD19-cretg were compared to two knockout mice: Traf2DB 80 and Traf3DB 94.  On Day 2 three control mice: Traf2lox/lox 77, Traf2lox/lox 79 and Traf3lox/lox 97 were compared to two knockout mice: Traf2DB 76 and Traf3DB 01.  On Day 3 three control mice: WT33, WT34, WT35 were compared to three Baff-tg mice: Baff-tg 99, Baff-tg 100, Baff-tg 101."
GSE10422_series_matrix.txtimp_info.txt
Traf3 r is 3 
Found knockout in !Series_overall_design	"Lymph node B cells were purified from Traf2 B cell knockout mice, Traf3 B cell knockout mice, Baff-tg mice and respective controls.  RNA was extracted and hybridised to Affymetrix 430 2.0 Mouse Genome Arrays.  Samples were processed and hence analysed on three spearate days.  Day 1 two control mice: Traf2lox/lox pool and CD19-cretg were compared to two knockout mice: Traf2DB 80 and Traf3DB 94.  On Day 2 three control mice: Traf2lox/lox 77, Traf2lox/lox 79 and Traf3lox/lox 97 were compared to two knockout mice: Traf2DB 76 and Traf3DB 01.  On Day 3 three control mice: WT33, WT34, WT35 were compared to three Baff-tg mice: Baff-tg 99, Baff-tg 100, Baff-tg 101."
GSE10422_series_matrix.txtimp_info.txt
NF r is 3 
Found activation in !Series_summary	"Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-κB2 (NF-κB2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family).  This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo.  We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling.  As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells.  This analysis should identify genes that are important in B cell survival."
GSE10424-GPL81_series_matrix.txtimp_info.txt
F10 r is 2 
Found + in !Series_summary	"The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum)."
GSE10424-GPL82_series_matrix.txtimp_info.txt
F10 r is 2 
Found + in !Series_summary	"The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum)."
GSE10424-GPL83_series_matrix.txtimp_info.txt
F10 r is 2 
Found + in !Series_summary	"The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum)."
GSE10430-GPL81_series_matrix.txtimp_info.txt
MyoD r is 1 
Found -/- in !Series_summary	"Note that the Triplicate1 sample = MyoD-/-1999; Triplicate 2 sample = MyoD-/-p6; Triplicate 3 sample = MyoD-/-p10."
GSE10430-GPL81_series_matrix.txtimp_info.txt
F10 r is 2 
Found + in !Series_summary	"The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum)."
GSE10430-GPL82_series_matrix.txtimp_info.txt
MyoD r is 1 
Found -/- in !Series_summary	"Note that the Triplicate1 sample = MyoD-/-1999; Triplicate 2 sample = MyoD-/-p6; Triplicate 3 sample = MyoD-/-p10."
GSE10430-GPL82_series_matrix.txtimp_info.txt
F10 r is 2 
Found + in !Series_summary	"The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum)."
GSE10430-GPL83_series_matrix.txtimp_info.txt
MyoD r is 1 
Found -/- in !Series_summary	"Note that the Triplicate1 sample = MyoD-/-1999; Triplicate 2 sample = MyoD-/-p6; Triplicate 3 sample = MyoD-/-p10."
GSE10430-GPL83_series_matrix.txtimp_info.txt
F10 r is 2 
Found + in !Series_summary	"The Differentiation is leaded by removing the Proliferation Medium (Ham's F10 Medium + growth factors) and feeding with Differentiation Medium (DMEM hg + 2.5% Horse serum)."
GSE10467_series_matrix.txtimp_info.txt
myeloid leukemia r is 8 
Found induced in !Series_summary	"Mammalian microRNAs (miRNAs) are emerging as key regulators of the development and function of the immune system. Here, we report a strong but transient induction of miR-155 in mouse bone marrow after injection of bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating the sufficiency of miR-155 to drive GM expansion, enforced expression in mouse bone marrow cells caused GM proliferation in a manner reminiscent of LPS treatment. However, the mir-155-induced GM populations displayed pathological features characteristic of myeloid neoplasia. Extending possible relevance to human disease, miR-155 was overexpressed in the bone marrow of patients with acute myeloid leukemia (AML). Furthermore, miR-155 repressed a subset of genes implicated in hematopoietic development and disease. These data implicate miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML, emphasizing the importance of proper miR-155 regulation in developing myeloid cells during times of inflammatory stress."
GSE10476_series_matrix.txtimp_info.txt
Ring1B r is 5 
Found KO in !Series_overall_design	"We observed gene expression of Ring1B single and Ring1A/B double KO cells using Affymetrix chip: MOE 430 2.0."
GSE10478_series_matrix.txtimp_info.txt
AAT r is 1 
Found treated in !Series_summary	"In this study, we performed the gene expression analysis of the Normal, Diabetic and AAT treated NOD mice to elucidate the transcriptional changes induced by AAT. This will assist in identifying the biological processes / pathways involved in curative mechanism of AAT."
GSE10478_series_matrix.txtimp_info.txt
AAT r is 1 
Found treated in !Series_overall_design	"Duplicate samples of Normal, Diabetic and AAT treated NOD mice were analyzed."
GSE10498-GPL339_series_matrix.txtimp_info.txt
Bax r is 1 
Found null in !Series_title	"Comparison of SCG expression profiles from Bax null versus NGF-Bax double null mice"
GSE10498-GPL339_series_matrix.txtimp_info.txt
SCG r is 5 
Found null in !Series_title	"Comparison of SCG expression profiles from Bax null versus NGF-Bax double null mice"
GSE10498-GPL339_series_matrix.txtimp_info.txt
Bax r is 3 
Found null in !Series_overall_design	"This experiment examine gene expression differences in superior cervical ganglia fro P0 bax null versus NGF-Bax double null animals. The Bax genotype was used in order to prevent the neuronal cell death normally observed in the NGF null animal."
GSE10498-GPL340_series_matrix.txtimp_info.txt
Bax r is 1 
Found null in !Series_title	"Comparison of SCG expression profiles from Bax null versus NGF-Bax double null mice"
GSE10498-GPL340_series_matrix.txtimp_info.txt
SCG r is 5 
Found null in !Series_title	"Comparison of SCG expression profiles from Bax null versus NGF-Bax double null mice"
GSE10498-GPL340_series_matrix.txtimp_info.txt
Bax r is 3 
Found null in !Series_overall_design	"This experiment examine gene expression differences in superior cervical ganglia fro P0 bax null versus NGF-Bax double null animals. The Bax genotype was used in order to prevent the neuronal cell death normally observed in the NGF null animal."
GSE10503_series_matrix.txtimp_info.txt
P17 r is 6 
Found loss of in !Series_title	"Identification of transcriptional changes due to loss of Hdac3 in liver at P17 and P28"
GSE10503_series_matrix.txtimp_info.txt
Hdac3 r is 2 
Found loss of in !Series_title	"Identification of transcriptional changes due to loss of Hdac3 in liver at P17 and P28"
GSE10503_series_matrix.txtimp_info.txt
Hdac3 r is 2 
Found knockout in !Series_summary	"Keywords: Genetic knockout of Hdac3 specifically in liver, and RNA analyzed from postnatal day 17 or 28 livers for transcriptional changes related to the given phenotypes"
GSE10503_series_matrix.txtimp_info.txt
Hdac3 r is 4 
Found expressing in !Series_overall_design	"Postnatal day 17 or 28 mice were used for the microarray analysis.  Total RNA was extracted from livers of either Hdac3 wild-type/heterozygous mice expressing Albumin-Cre or Hdac3-null livers, and pooled together in groups of 5.  One pool of control or Hdac3-null liver RNA from both time points was used in technical replicates, meaning each sample was run in duplicate on separate lots of microarray chips to determine reproducibility of the Applied Biosystems ABI1700 chips.  The second set of RNA pools were used as biological replicates for each group at each time point."
GSE10516_series_matrix.txtimp_info.txt
Lmx1b r is 2 
Found lacking in !Series_summary	"A control vs. genetic knockout experiment aimed at determining what RNAs are upregulated or downregulated in e11.5 mouse proximal limb tissue lacking the Lmx1b gene.  Because Lmx1b is required for dorsal-ventral patterning of the limb, this screen gives insight into what putative downstream targets of Lmx1b contribute to dorsal-ventral patterning."
GSE10519_series_matrix.txtimp_info.txt
Dnmt1 r is 1 
Found KO in !Series_overall_design	"Gene expression in Dnmt1-KO cells were observed using Affymetrix chip: MOE 430 2.0."
GSE10534_series_matrix.txtimp_info.txt
Gata6 r is 1 
Found overexpression in !Series_title	"Gene expression of mouse ES cells in Gata6 overexpression experiments"
GSE10555_series_matrix.txtimp_info.txt
Slc39a13 r is 1 
Found knockout in !Series_title	"Comparision of expression profile between wild-type and Slc39a13 knockout osteoblasts"
GSE10556_series_matrix.txtimp_info.txt
Slc39a13 r is 1 
Found knockout in !Series_title	"Comparision of expression profile between wild-type and Slc39a13 knockout chondrocytes"
GSE10573-GPL1261_series_matrix.txtimp_info.txt
Ring1A r is 6 
Found KO in !Series_overall_design	"ChIP-chip experiments (GSM266076 and GSM266077) revealed the Ring1B-binding sites in promoter regions in ES cells. Microarray experiments were also performed (GSM265040 and GSM265041 for Ring1B KO, GSM265042 and GSM265043 for Ring1A and Ring1B double KO, and GSM265044, GSM265045 and GSM266115 for Oct3/4 KO)."
GSE10573-GPL4128_series_matrix.txtimp_info.txt
Ring1A r is 6 
Found KO in !Series_overall_design	"ChIP-chip experiments (GSM266076 and GSM266077) revealed the Ring1B-binding sites in promoter regions in ES cells. Microarray experiments were also performed (GSM265040 and GSM265041 for Ring1B KO, GSM265042 and GSM265043 for Ring1A and Ring1B double KO, and GSM265044, GSM265045 and GSM266115 for Oct3/4 KO)."
GSE10574_series_matrix.txtimp_info.txt
Eed r is 1 
Found KO in !Series_overall_design	"We generated constitutive Eed KO mouse ES cells and observed gene expression using Affymetrix MOE430.2 microarray."
GSE10574_series_matrix.txtimp_info.txt
Ring1A r is 6 
Found KO in !Series_overall_design	"These results were compared with other KO cells of PRC1 proteins (Ring1A, Ring1B) and other proteins in our study."
GSE10574_series_matrix.txtimp_info.txt
Ring1B r is 8 
Found KO in !Series_overall_design	"These results were compared with other KO cells of PRC1 proteins (Ring1A, Ring1B) and other proteins in our study."
GSE10587_series_matrix.txtimp_info.txt
pendrin r is 6 
Found knockout in !Series_summary	"Determination of differential expression of genes in the stria vascularis of  pendrin (Slc26a4) heterozygous and knockout  mice before the onset of hearing at postnatal day 10 (P10)."
GSE10587_series_matrix.txtimp_info.txt
Slc26a4 r is 4 
Found knockout in !Series_summary	"Determination of differential expression of genes in the stria vascularis of  pendrin (Slc26a4) heterozygous and knockout  mice before the onset of hearing at postnatal day 10 (P10)."
GSE10587_series_matrix.txtimp_info.txt
pendrin r is 6 
Found knockout in !Series_overall_design	"A total of Six samples  of stria vascularis RNA obtained from P10 mice were analyzed.  Triplicates from  pendrin (Slc26a4) heterozygous and knockout mice were run and analyzed."
GSE10587_series_matrix.txtimp_info.txt
Slc26a4 r is 4 
Found knockout in !Series_overall_design	"A total of Six samples  of stria vascularis RNA obtained from P10 mice were analyzed.  Triplicates from  pendrin (Slc26a4) heterozygous and knockout mice were run and analyzed."
GSE10587_series_matrix.txtimp_info.txt
Slc26a4 r is 1 
Found lacking in !Series_title	"Gene expression in stria vascularis of mice lacking Slc26a4 and heterzygous controls before the onset of hearing."
GSE10589_series_matrix.txtimp_info.txt
pendrin r is 6 
Found knockout in !Series_summary	"Determination of differential expression of genes in the thyroid of pendrin (Slc26a4) heterozygous and knockout mice at a time point corresponding to maximal thyroid gland activity, postnatal day 15 (P15). "
GSE10589_series_matrix.txtimp_info.txt
Slc26a4 r is 4 
Found knockout in !Series_summary	"Determination of differential expression of genes in the thyroid of pendrin (Slc26a4) heterozygous and knockout mice at a time point corresponding to maximal thyroid gland activity, postnatal day 15 (P15). "
GSE10589_series_matrix.txtimp_info.txt
pendrin r is 6 
Found knockout in !Series_overall_design	"A total of Six samples of thyroid RNA obtained from P15 mice were analyzed. Triplicates from pendrin (Slc26a4) heterozygous and knockout mice were run and analyzed."
GSE10589_series_matrix.txtimp_info.txt
Slc26a4 r is 4 
Found knockout in !Series_overall_design	"A total of Six samples of thyroid RNA obtained from P15 mice were analyzed. Triplicates from pendrin (Slc26a4) heterozygous and knockout mice were run and analyzed."
GSE10589_series_matrix.txtimp_info.txt
Slc26a4 r is 1 
Found lacking in !Series_title	"Comparison of gene expression between the thyroid of mice lacking Slc26a4 and heterzygous controls."
GSE10628_series_matrix.txtimp_info.txt
Foxj3 r is 1 
Found KO in !Series_summary	"Myoblasts harvested from a postnatal day 2 WT and Foxj3 KO litter."
GSE10628_series_matrix.txtimp_info.txt
Foxj3 r is 1 
Found mutant in !Series_summary	"We used Affymetrix microarrays to identify dysregulated transcripts in Foxj3 mutant myoblasts."
GSE10640-GPL4783_series_matrix.txtimp_info.txt
PB r is 7 
Found exposure in !Series_overall_design	"We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses.  Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy).   A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100% specific at distinguishing irradiated from septic animals.  We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90% and 81%, respectively."
GSE10640-GPL6524_series_matrix.txtimp_info.txt
PB r is 7 
Found exposure in !Series_overall_design	"We have sought to determine the impact of several variables on the PB gene expression profile of an environmental exposure, ionizing radiation, and to determine the specificity of the PB signature of radiation versus other genotoxic stresses.  Neither genotype differences nor the time of PB sampling caused any lessening of the accuracy of PB signatures to predict radiation exposure, but sex difference did influence the accuracy of the prediction of radiation exposure at the lowest level (50 cGy).   A PB signature of sepsis was also generated and both the PB signature of radiation and the PB signature of sepsis were found to be 100% specific at distinguishing irradiated from septic animals.  We also identified human PB signatures of radiation exposure and chemotherapy treatment which distinguished irradiated patients and chemotherapy-treated individuals within a heterogeneous population with accuracies of 90% and 81%, respectively."
GSE10659_series_matrix.txtimp_info.txt
cubilin r is 5 
Found knockout in !Series_summary	"Keywords: reduced folate carrier knockout, folate receptor, cubilin, megalin, embryos, gene expression, neural tube defect, chorioallantoic fusion"
GSE10659_series_matrix.txtimp_info.txt
RFC r is 2 
Found KO in !Series_title	"AFFYMETRIX ANALYSIS OF E9.5 RFC MOUSE KO EMBRYOS REVEALS ALTERED EXPR’N OF GENES IN THE CUBILIN-MEGALIN COMPLEX"
GSE10659_series_matrix.txtimp_info.txt
RFC r is 1 
Found KO in !Series_summary	"Comparison of RFC KO, wildtype normal embryos vs. RFC KO, nullizygous affected embryos"
GSE10659_series_matrix.txtimp_info.txt
RFC r is 1 
Found KO in !Series_overall_design	"6 samples RFC KO mouse embryos, E9.5, folic acid treated: 3 Control, Wildtype, normal; 3 Affected, Nullizygous, CR/chorioallantoic defect; as paired-littermates with one normal and one affected embryo per set from each of three separate litters for RNA extraction and hybridization on Affymetrix microarrays."
GSE10684_series_matrix.txtimp_info.txt
Mdr1a r is 1 
Found -/- in !Series_summary	"Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARalpha activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation."
GSE10684_series_matrix.txtimp_info.txt
PXR r is 3 
Found activation in !Series_summary	"Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARalpha activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation."
GSE10684_series_matrix.txtimp_info.txt
PPARalpha r is 1 
Found activation in !Series_summary	"Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARalpha activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation."
GSE10726_series_matrix.txtimp_info.txt
beta-catenin r is 2 
Found mutant in !Series_title	"Expression data from skin of epithelial activated beta-catenin mutant mouse embryo"
GSE10726_series_matrix.txtimp_info.txt
Ctnnb1 r is 3 
Found mutant in !Series_overall_design	"Appended below is Table S3: Full list of differentially expressed genes in KRT14-Cre Ctnnb1(Ex3)fl/+ mutant compared with control littermate intact skin at E14.5, including normalization and filter parameters. Fold change, listed in the second column, gives the ratio of normalized mutant : control transcript levels."
GSE10727_series_matrix.txtimp_info.txt
beta-catenin r is 2 
Found mutant in !Series_title	"Expression data from dermis of epithelial activated beta-catenin mutant mouse embryo"
GSE10727_series_matrix.txtimp_info.txt
Ctnnb1 r is 3 
Found mutant in !Series_overall_design	"Appended below is Table S2: Full list of differentially expressed genes in KRT14-Cre Ctnnb1(Ex3)fl/+ mutant compared with control littermate dermis at E15.5, including normalization and filter parameters. Fold change, listed in the second column, gives the ratio of normalized mutant : control transcript levels."
GSE10728_series_matrix.txtimp_info.txt
beta-catenin r is 2 
Found mutant in !Series_title	"Expression data from epidermis of epithelial activated beta-catenin mutant mouse embryo"
GSE10728_series_matrix.txtimp_info.txt
Ctnnb1 r is 3 
Found mutant in !Series_overall_design	"Appended below is Table S1: Full list of differentially expressed genes in KRT14-Cre Ctnnb1(Ex3)fl/+ mutant compared with control littermate epidermis at E15.5, including normalization and filter parameters. Fold change, listed in the second column, gives the ratio of normalized control : mutant transcript levels."
GSE10733_series_matrix.txtimp_info.txt
beta-catenin r is 2 
Found mutant in !Series_title	"Expression data from skin, dermis, and epidermis of epithelial activated beta-catenin mutant mouse embryo"
GSE10740_series_matrix.txtimp_info.txt
Slc9a3 r is 4 
Found deficient in !Series_title	"Expression data from  the colon of wild-type and Slc9a3 (NHE3)-deficient mice"
GSE10740_series_matrix.txtimp_info.txt
NHE3 r is 2 
Found deficient in !Series_title	"Expression data from  the colon of wild-type and Slc9a3 (NHE3)-deficient mice"
GSE10740_series_matrix.txtimp_info.txt
NHE3 r is 1 
Found deficient in !Series_overall_design	"Whole colon was dissected from 6-8 week old NHE3-deficient mice and their wild-type littermates and total RNA isolated for microarray analysis using Affymetrix murine MOE430 2.0 arrays"
GSE10743_series_matrix.txtimp_info.txt
PTC r is 5 
Found induced in !Series_summary	"The RET/PTC3 (RP3) fusion gene is the most frequent mutation found in radiation-induced papillary thyroid cancers (PTC). Several studies suggest that the RET/PTC rearrangement is an initiating event in tumorigenesis. E7 is an oncoprotein derived from the Human Papilllomavirus 16 (HPV16) responsible for most cervical carcinoma in women. We studied here the sequence of events leading to thyroid cancer in Tg-RP3 and Tg-E7 mice expressing the transgene exclusively in the thyroid under the control of thyroglobulin (Tg) promoter. Both transgenic mice develop thyroid hyperplasia followed by solid differentiated carcinoma in older animals. To understand the different steps leading to carcinoma, we analyzed thyroid gene expression in both strains at different ages (2, 6, 10 months) by microarray technology. Important biological processes were differentially regulated in the two tumor types. In E7 thyroids cell cycle was the most upregulated process; observation consistent with the huge size of these tumors. In RP3 thyroids immunity was the most significantly regulated process, as previously observed in microarray data on human PTC. Interestingly, other human PTC characteristics were also observed in RP3 but not in E7 mouse tumors: similar regulation of several human PTC markers, upregulation of many EGF-like growth factors and finally significant regulation of angiogenesis and extracellular matrix remodeling-related genes. In summary we showed that RP3 contrary to E7 mouse tumors share several important genotypic characteristics with human PTC, observation reinforcing the validity of this model to study human thyroid tumorigenesis.  "
GSE10743_series_matrix.txtimp_info.txt
Tg r is 6 
Found expressing in !Series_summary	"The RET/PTC3 (RP3) fusion gene is the most frequent mutation found in radiation-induced papillary thyroid cancers (PTC). Several studies suggest that the RET/PTC rearrangement is an initiating event in tumorigenesis. E7 is an oncoprotein derived from the Human Papilllomavirus 16 (HPV16) responsible for most cervical carcinoma in women. We studied here the sequence of events leading to thyroid cancer in Tg-RP3 and Tg-E7 mice expressing the transgene exclusively in the thyroid under the control of thyroglobulin (Tg) promoter. Both transgenic mice develop thyroid hyperplasia followed by solid differentiated carcinoma in older animals. To understand the different steps leading to carcinoma, we analyzed thyroid gene expression in both strains at different ages (2, 6, 10 months) by microarray technology. Important biological processes were differentially regulated in the two tumor types. In E7 thyroids cell cycle was the most upregulated process; observation consistent with the huge size of these tumors. In RP3 thyroids immunity was the most significantly regulated process, as previously observed in microarray data on human PTC. Interestingly, other human PTC characteristics were also observed in RP3 but not in E7 mouse tumors: similar regulation of several human PTC markers, upregulation of many EGF-like growth factors and finally significant regulation of angiogenesis and extracellular matrix remodeling-related genes. In summary we showed that RP3 contrary to E7 mouse tumors share several important genotypic characteristics with human PTC, observation reinforcing the validity of this model to study human thyroid tumorigenesis.  "
GSE10745_series_matrix.txtimp_info.txt
histone H3 r is 6 
Found treated in !Series_summary	"Methodology/Principal Findings: By chromatin immunoprecipitation, we detected the same heterochromatin marks in homozygous mice carrying a (GAA)230 repeat in the first intron of the mouse frataxin gene (KIKI mice). These animals have decreased frataxin levels and, by microarray analysis, show significant gene expression changes in several tissues. We treated KIKI mice with a novel histone deacetylase inhibitor, compound 106, which substantially increases frataxin mRNA levels in cells from Friedreich ataxia individuals. Treatment increased histone H3 and H4 acetylation in chromatin near the GAA repeat and restored wild-type frataxin levels in the nervous system and heart, as determined by quantitative RT-PCR and semiquantitative western blot analysis. No toxicity was observed. Furthermore, most of the differentially expressed genes in KIKI mice reverted towards wild-type levels. "
GSE10765_series_matrix.txtimp_info.txt
IRAK r is 2 
Found -/- in !Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"
GSE10765_series_matrix.txtimp_info.txt
IRAK-1 r is 2 
Found -/- in !Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"
GSE10765_series_matrix.txtimp_info.txt
IRAK-2 r is 2 
Found -/- in !Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"
GSE10765_series_matrix.txtimp_info.txt
IRAK r is 2 
Found -/- in !Series_overall_design	"Peritoneal macrophages from wild-type, IRAK-2-/- and IRAK-1/IRAK-2 mice were stimulated with MALP-2 for 0, 2, 4, and 8 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."
GSE10765_series_matrix.txtimp_info.txt
IRAK-2 r is 2 
Found -/- in !Series_overall_design	"Peritoneal macrophages from wild-type, IRAK-2-/- and IRAK-1/IRAK-2 mice were stimulated with MALP-2 for 0, 2, 4, and 8 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."
GSE10765_series_matrix.txtimp_info.txt
IRAK r is 6 
Found stimulated in !Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"
GSE10765_series_matrix.txtimp_info.txt
IRAK-1 r is 6 
Found stimulated in !Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"
GSE10765_series_matrix.txtimp_info.txt
IRAK-2 r is 6 
Found stimulated in !Series_title	"Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice"
GSE10796_series_matrix.txtimp_info.txt
leukemia inhibitory factor r is 7 
Found stimulated in !Series_summary	"During development of the mammalian central nervous system (CNS), neurons and glial cells (astrocytes and oligodendrocytes) are generated from common neural precursor cells (NPCs). However, neurogenesis precedes gliogenesis, which normally commences at later stages of fetal telencephalic development. Astrocyte differentiation of mouse NPCs at embryonic day (E) 14.5 (relatively late gestation) is induced by activation of the transcription factor STAT3, whereas at E11.5 (mid-gestation) NPCs do not differentiate into astrocytes even when stimulated by STAT3-activating cytokines such as leukemia inhibitory factor (LIF). This can be explained in part by the fact that astrocyte-specific gene promoters are highly methylated in NPCs at E11.5, but other mechanisms are also likely to play a role. We therefore sought to identify genes involved in the inhibition of astrocyte differentiation of NPCs at midgestation. We first examined gene expression profiles in E11.5 and E14.5 NPCs, using Affymetrix GeneChip analysis, applying the Percellome method to normalize gene expression level. We then conducted in situ hybridization analysis for selected genes found to be highly expressed in NPCs at midgestation. Among these genes, we found that N-myc and high mobility group AT-hook 2 (Hmga2) were highly expressed in the E11.5 but not the E14.5 ventricular zone of mouse brain, where NPCs reside. Transduction of N-myc and Hmga2 by retroviruses into E14.5 NPCs, which normally differentiate into astrocytes in response to LIF, resulted in suppression of astrocyte differentiation. However, sustained expression of N-myc and Hmga2 in E11.5 NPCs failed to maintain the hypermethylated status of an astrocyte-specific gene promoter. Taken together, our data suggest that astrocyte differentiation of NPCs is regulated not only by DNA methylation but also by genes whose expression is controlled spatio-temporally during brain development."
GSE10807_series_matrix.txtimp_info.txt
Atm r is 1 
Found deficient in !Series_title	"Expression profiling of Atm deficient murine thymic lymphoma"
GSE10807_series_matrix.txtimp_info.txt
Atm r is 1 
Found deficient in !Series_summary	"To find genes deregulated in the pathogenisis of T-cells in Atm deficient mice, we performed expression profiling of Atm deficient thymic lymphomas, wildtype thymi and Atm deficient thymi without macroscopic enlargement, representing an intermediate stage in the process of tumorigenisis."
GSE10807_series_matrix.txtimp_info.txt
Atm r is 1 
Found deficient in !Series_overall_design	"To evaluate differential gene expression of Atm deficient thymic lymphoma we performed microarray based expression profiling of 8 Atm deficient thymic lymphomas, 6 wildtype thymi, 1 thymus of an Atm heterozygous mouse and 18 thymi of Atm deficient mice without  macroscopic enlargement."
GSE10817_series_matrix.txtimp_info.txt
Mll5 r is 1 
Found -/- in !Series_overall_design	"Bone marrow cells were pooled from 6 pairs of eight weeks old Mll5-/- mice and sex matched wild type littermates, and then were stained with a cocktail of biotinylated anti-mouse lineage antibodies to CD3, CD4, CD5, CD8, B220, CD11b, Gr-1 and Ter119 (eBioscience). For detection and sorting, we used Streptavidin conjugated with PE-Cy7, anti-Sca-1-APC and c-Kit-APC-Alexa F750 antibodies (eBioscience). 2.5 × 105 LSK (Lin-, Sca-1+, c-kit+) cells were flow sorted. Total RNA (320 ng) was isolated by using RNeasy Mini kit (Qiagen) following the manufactures instruction. RNA amplification and array hybridization were performed in UCSF Shared Microarray Core Facilities. Briefly, total RNA quality was assessed using a Pico Chip on an Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). RNA was amplified and labeled with Cy3-CTP using the Agilent low RNA input fluorescent linear amplification kits following the manufacturers protocol (Agilent). Labeled cRNA was assessed using the Nandrop ND-100 (Nanodrop Technologies, Inc., Wilmington DE), and equal amounts of Cy3 labeled target were hybridized to Agilent whole mouse genome 4x44K Ink-jet arrays (Agilent). Hybridizations were performed for 14 hours, according to the manufacturers protocol (Agilent). Arrays were scanned using the Agilent microarray scanner (Agilent) and raw signal intensities were extracted with Feature Extraction v9.1 software (Agilent,)."
GSE10866_series_matrix.txtimp_info.txt
Mlh1 r is 1 
Found -/- in !Series_overall_design	"RNA was extracted from uterine segments with either CAH or invasive carcinoma from  Pten+/-;Mlh1-/- , Pten+/-;Mlh1+/+ and Wild type female mice. The RNA was hybridized to Affymetrix mouse 430A chip in order to determine changes in global gene expression patterns"
GSE10869_series_matrix.txtimp_info.txt
CaMKIV r is 2 
Found loss of in !Series_summary	"Our goal was to analyze how loss of CaMKIV will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine."
GSE10869_series_matrix.txtimp_info.txt
CaMKIV r is 4 
Found induced in !Series_title	"Effects of CaMKIV loss on cocaine-induced gene expression in the striatum"
GSE10869_series_matrix.txtimp_info.txt
CaMKIV r is 6 
Found induced in !Series_summary	"Our goal was to analyze how loss of CaMKIV will affect acitivity-regulated transcription induced by strong stimulation, i.e. cocaine."
GSE10895_series_matrix.txtimp_info.txt
multifunctional protein 2 r is 3 
Found deficient in !Series_summary	"Study on gene expression in multifunctional protein 2 deficient mice. Liver samples of two days old mice in normal conditions are used. In total 8 arrays were hybridized corresponding to 4 KO mice and 4 WT mice Results: Cholesterol synthesis is induced and ppar alpha targets also differentially expressed between KO and WT."
GSE10902_series_matrix.txtimp_info.txt
Rb r is 7 
Found null in !Series_summary	"The LIM-only protein FHL2 acts as a transcriptional modulator that positively or negatively regulates multiple signaling pathways. We recently reported that FHL2 cooperates with CBP/p300 in the activation of ß-catenin/TCF target gene cyclin D1. In this paper, we demonstrate that FHL2 is associated with the cyclin D1 promoter at the TCF/CRE site, providing evidence that cyclin D1 is a direct target of FHL2. We show that deficiency of FHL2 greatly reduces the proliferative capacity of spontaneously immortalized mouse fibroblasts which is associated with decreased expression of cyclin D1 and p16INK4a, and hypophosphorylation of Rb. Reexpression of FHL2 in FHL2-null fibroblasts efficiently restores cyclin D1 levels and cell proliferative capacity, indicating that FHL2 is critical for cyclin D1 activation and cell growth. Moreover, ectopic cyclin D1 expression is sufficient to override growth inhibition of immortalized FHL2-null fibroblasts. Gene expression profiling revealed that FHL2 deficiency triggers a broad change of the cell cycle program that is associated with downregulation of several G1/S and G2/M cyclins, E2F transcription factors and DNA replication machinery, thus correlating with reduced cell proliferation. This change also involves downregulation of the negative cell cycle regulators, particularly INK4 inhibitors, which could counteract the decreased expression of cyclins, allowing cells to grow. Our study illustrates that FHL2 can act on different aspects of the cell cycle program to finely regulate cell proliferation."
GSE10902_series_matrix.txtimp_info.txt
cyclin r is 6 
Found activation in !Series_summary	"The LIM-only protein FHL2 acts as a transcriptional modulator that positively or negatively regulates multiple signaling pathways. We recently reported that FHL2 cooperates with CBP/p300 in the activation of ß-catenin/TCF target gene cyclin D1. In this paper, we demonstrate that FHL2 is associated with the cyclin D1 promoter at the TCF/CRE site, providing evidence that cyclin D1 is a direct target of FHL2. We show that deficiency of FHL2 greatly reduces the proliferative capacity of spontaneously immortalized mouse fibroblasts which is associated with decreased expression of cyclin D1 and p16INK4a, and hypophosphorylation of Rb. Reexpression of FHL2 in FHL2-null fibroblasts efficiently restores cyclin D1 levels and cell proliferative capacity, indicating that FHL2 is critical for cyclin D1 activation and cell growth. Moreover, ectopic cyclin D1 expression is sufficient to override growth inhibition of immortalized FHL2-null fibroblasts. Gene expression profiling revealed that FHL2 deficiency triggers a broad change of the cell cycle program that is associated with downregulation of several G1/S and G2/M cyclins, E2F transcription factors and DNA replication machinery, thus correlating with reduced cell proliferation. This change also involves downregulation of the negative cell cycle regulators, particularly INK4 inhibitors, which could counteract the decreased expression of cyclins, allowing cells to grow. Our study illustrates that FHL2 can act on different aspects of the cell cycle program to finely regulate cell proliferation."
GSE10902_series_matrix.txtimp_info.txt
cyclin D1 r is 6 
Found activation in !Series_summary	"The LIM-only protein FHL2 acts as a transcriptional modulator that positively or negatively regulates multiple signaling pathways. We recently reported that FHL2 cooperates with CBP/p300 in the activation of ß-catenin/TCF target gene cyclin D1. In this paper, we demonstrate that FHL2 is associated with the cyclin D1 promoter at the TCF/CRE site, providing evidence that cyclin D1 is a direct target of FHL2. We show that deficiency of FHL2 greatly reduces the proliferative capacity of spontaneously immortalized mouse fibroblasts which is associated with decreased expression of cyclin D1 and p16INK4a, and hypophosphorylation of Rb. Reexpression of FHL2 in FHL2-null fibroblasts efficiently restores cyclin D1 levels and cell proliferative capacity, indicating that FHL2 is critical for cyclin D1 activation and cell growth. Moreover, ectopic cyclin D1 expression is sufficient to override growth inhibition of immortalized FHL2-null fibroblasts. Gene expression profiling revealed that FHL2 deficiency triggers a broad change of the cell cycle program that is associated with downregulation of several G1/S and G2/M cyclins, E2F transcription factors and DNA replication machinery, thus correlating with reduced cell proliferation. This change also involves downregulation of the negative cell cycle regulators, particularly INK4 inhibitors, which could counteract the decreased expression of cyclins, allowing cells to grow. Our study illustrates that FHL2 can act on different aspects of the cell cycle program to finely regulate cell proliferation."
GSE10902_series_matrix.txtimp_info.txt
CBP/p300 r is 3 
Found activation in !Series_summary	"The LIM-only protein FHL2 acts as a transcriptional modulator that positively or negatively regulates multiple signaling pathways. We recently reported that FHL2 cooperates with CBP/p300 in the activation of ß-catenin/TCF target gene cyclin D1. In this paper, we demonstrate that FHL2 is associated with the cyclin D1 promoter at the TCF/CRE site, providing evidence that cyclin D1 is a direct target of FHL2. We show that deficiency of FHL2 greatly reduces the proliferative capacity of spontaneously immortalized mouse fibroblasts which is associated with decreased expression of cyclin D1 and p16INK4a, and hypophosphorylation of Rb. Reexpression of FHL2 in FHL2-null fibroblasts efficiently restores cyclin D1 levels and cell proliferative capacity, indicating that FHL2 is critical for cyclin D1 activation and cell growth. Moreover, ectopic cyclin D1 expression is sufficient to override growth inhibition of immortalized FHL2-null fibroblasts. Gene expression profiling revealed that FHL2 deficiency triggers a broad change of the cell cycle program that is associated with downregulation of several G1/S and G2/M cyclins, E2F transcription factors and DNA replication machinery, thus correlating with reduced cell proliferation. This change also involves downregulation of the negative cell cycle regulators, particularly INK4 inhibitors, which could counteract the decreased expression of cyclins, allowing cells to grow. Our study illustrates that FHL2 can act on different aspects of the cell cycle program to finely regulate cell proliferation."
GSE10902_series_matrix.txtimp_info.txt
D1 r is 7 
Found activation in !Series_summary	"The LIM-only protein FHL2 acts as a transcriptional modulator that positively or negatively regulates multiple signaling pathways. We recently reported that FHL2 cooperates with CBP/p300 in the activation of ß-catenin/TCF target gene cyclin D1. In this paper, we demonstrate that FHL2 is associated with the cyclin D1 promoter at the TCF/CRE site, providing evidence that cyclin D1 is a direct target of FHL2. We show that deficiency of FHL2 greatly reduces the proliferative capacity of spontaneously immortalized mouse fibroblasts which is associated with decreased expression of cyclin D1 and p16INK4a, and hypophosphorylation of Rb. Reexpression of FHL2 in FHL2-null fibroblasts efficiently restores cyclin D1 levels and cell proliferative capacity, indicating that FHL2 is critical for cyclin D1 activation and cell growth. Moreover, ectopic cyclin D1 expression is sufficient to override growth inhibition of immortalized FHL2-null fibroblasts. Gene expression profiling revealed that FHL2 deficiency triggers a broad change of the cell cycle program that is associated with downregulation of several G1/S and G2/M cyclins, E2F transcription factors and DNA replication machinery, thus correlating with reduced cell proliferation. This change also involves downregulation of the negative cell cycle regulators, particularly INK4 inhibitors, which could counteract the decreased expression of cyclins, allowing cells to grow. Our study illustrates that FHL2 can act on different aspects of the cell cycle program to finely regulate cell proliferation."
GSE10904_series_matrix.txtimp_info.txt
Pdss2 r is 1 
Found knockout in !Series_title	"Expression data from wildtype and alb/cre liver-conditional Pdss2 knockout mutant mice"
GSE10904_series_matrix.txtimp_info.txt
Pdss2 r is 3 
Found knockout in !Series_summary	"Utilizing M. musculus as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease.  We characterized genome-wide expression profiles of liver-conditional knockout mice for Pdss2 compared with loxP controls."
GSE10904_series_matrix.txtimp_info.txt
Pdss2 r is 2 
Found mutant in !Series_title	"Expression data from wildtype and alb/cre liver-conditional Pdss2 knockout mutant mice"
GSE10908_series_matrix.txtimp_info.txt
dn r is 2 
Found mutant in !Series_summary	"To assess the influence of ADAM10 on the gene expression profile in the brain we performed microarray analysis using RNA isolated from brains of five month old mice over-expressing either the α-secretase ADAM10 or a dominant-negative mutant (dn) of this enzyme. As compared to non-transgenic wild-type mice, 355 genes were found to be differentially expressed in ADAM10 transgenic mice and 143 genes in dnADAM10 mice. A higher number of genes was found to be differentially regulated in double-transgenic mouse strains additionally expressing the human APP V717I mutant (APP[V717I]). Thus, α-secretase cleavage of over-expressed APP[V717I] alters CNS gene expression additionally."
GSE10915_series_matrix.txtimp_info.txt
leptin r is 1 
Found treated in !Series_title	"Comparative analysis of gene expression in ob/ob leptin-treated and ob/ob saline-treated lungs."
GSE10941_series_matrix.txtimp_info.txt
Mxi1 r is 1 
Found deficient in !Series_title	"Confirmation of the gene expression pattern in Mxi1-deficient mouse (time course)"
GSE10941_series_matrix.txtimp_info.txt
Mxi1 r is 1 
Found KO in !Series_summary	"For final aim to completes network map between gene that is concerned in cystogenesis, verifies meaning genes connected with cyst formation analyzing gene pattern in time-dependent Mxi1 KO mouse that have phenotype of polycystic kidney disease. Monitoring meaning genes through microarray analysis, and confirm the function of these genes. Also, find pathway including meaning genes and new pathway related with PKD. Completes network map concerned in time-dependent cystogenesis through integrates knowing pathway and predicting pathway. Develope diagnostic of cyst disease and cure target through such completed network map, and wish to clear new role of cyst formation connection gene through in vivo model and examine closely control system of cyst formation mechanism. "
GSE10989_series_matrix.txtimp_info.txt
Fh1 r is 1 
Found knockout in !Series_summary	"We used microarrays to detail the global programme of gene  expression underlying cyst development in Fh1 knockout mice and identified distinct classes of up-regulated genes during this process."
GSE10989_series_matrix.txtimp_info.txt
Fh1 r is 1 
Found knockout in !Series_overall_design	"Renal epithelial tissue was macro-dissected from Fh1 knockout mice and sex-matched litter mate control disease-free animals for RNA extraction and hybridization on Affymetrix microarrays."
GSE11005_series_matrix.txtimp_info.txt
CD40 ligand r is 2 
Found knock-out in !Series_summary	"Pneumocystis is a pathogen of immunocompromised hosts but can also infect healthy hosts, in whom infection is rapidly controlled and cleared. To better understand the immune mechanisms contributing to clearance of infection, microarray methods were used to examine differential gene expression in the lungs of  C57BL/6 and CD40 ligand knock-out (CD40L-KO) mice over time following exposure to Pneumocystis. Immuncompetent C57BL/6 mice, which control and clear infection efficiently, showed a robust response to infection characterized by the upregulation of 349 primarily immune-response associated genes.  Temporal changes in the expression of these genes suggested that there was an early (week 2) primarily innate response, that waned without controlling infection; this were followed by primarily adaptive immune responses that peaked at week 5 and successfully cleared the infection. In conjunction with the latter, there was an increased expression of B cell associated (immunoglobulin) genes at week 6 that persisted through 11 weeks.   In contrast, CD40L-KO mice, which are highly susceptible to developing severe Pneumocystis pneumonia, showed essentially no upregulation of immune-response associated genes at days 35 to 75. Immunohistochemical staining supported these observations by demonstrating an increase in CD4+, CD68+, and CD19+ cells in C57BL/6 but not CD40L-KO mice. Thus, the healthy host demonstrates a robust biphasic response to infection by Pneumocystis; CD40 ligand is an essential upstream regulator of the adaptive immune responses that efficiently control infection and prevent development of progressive pneumonia."
GSE11005_series_matrix.txtimp_info.txt
CD40 ligand r is 6 
Found KO in !Series_summary	"Pneumocystis is a pathogen of immunocompromised hosts but can also infect healthy hosts, in whom infection is rapidly controlled and cleared. To better understand the immune mechanisms contributing to clearance of infection, microarray methods were used to examine differential gene expression in the lungs of  C57BL/6 and CD40 ligand knock-out (CD40L-KO) mice over time following exposure to Pneumocystis. Immuncompetent C57BL/6 mice, which control and clear infection efficiently, showed a robust response to infection characterized by the upregulation of 349 primarily immune-response associated genes.  Temporal changes in the expression of these genes suggested that there was an early (week 2) primarily innate response, that waned without controlling infection; this were followed by primarily adaptive immune responses that peaked at week 5 and successfully cleared the infection. In conjunction with the latter, there was an increased expression of B cell associated (immunoglobulin) genes at week 6 that persisted through 11 weeks.   In contrast, CD40L-KO mice, which are highly susceptible to developing severe Pneumocystis pneumonia, showed essentially no upregulation of immune-response associated genes at days 35 to 75. Immunohistochemical staining supported these observations by demonstrating an increase in CD4+, CD68+, and CD19+ cells in C57BL/6 but not CD40L-KO mice. Thus, the healthy host demonstrates a robust biphasic response to infection by Pneumocystis; CD40 ligand is an essential upstream regulator of the adaptive immune responses that efficiently control infection and prevent development of progressive pneumonia."
GSE11035_series_matrix.txtimp_info.txt
5HTT r is 8 
Found loss of in !Series_overall_design	"Comparison of whole lung total RNA from pools of wild-type, heterozygote, and knockout 5HTT mice to determine the pulmonary effects of loss of 5HTT expression."
GSE11035_series_matrix.txtimp_info.txt
5HTT r is 1 
Found knockout in !Series_title	"Effect of 5HTT knockout and heterozygosity in whole mouse lung"
GSE11035_series_matrix.txtimp_info.txt
5HTT r is 1 
Found knockout in !Series_overall_design	"Comparison of whole lung total RNA from pools of wild-type, heterozygote, and knockout 5HTT mice to determine the pulmonary effects of loss of 5HTT expression."
GSE11035_series_matrix.txtimp_info.txt
5-HTT r is 2 
Found knock-out in !Series_summary	"Rationale: While modulation of the serotonin transporter (5HTT) has shown to be a risk factor for pulmonary arterial hypertension for almost 40 years, there is a lack of in vivo data about the broad molecular effects of pulmonary inhibition of 5HTT. Previous studies have suggested effects on inflammation, proliferation, and vasoconstriction. The goal of this study was to determine which of these were supported by alterations in gene expression in serotonin transporter knockout mice. Methods: Eight week old normoxic mice with a 5-HTT knock-out (5HTT-/-) and their heterozygote(5HTT+/-) or wild-type(5HTT+/+) littermates had right ventricular systolic pressure(RVSP) assessed, lungs collected for RNA, pooled, and used in duplicate in Affymetrix array analysis. Representative genes were confirmed by quantitative RT-PCR and western blot. Results: RVSP was normal in all groups. Only 124 genes were reliably changed between 5HTT-/- and 5HTT+/+ mice. More than half of these were either involved in inflammatory response or muscle function and organization; in addition, some matrix, heme oxygenase, developmental, and energy metabolism genes showed altered expression. Quantitative RT-PCR for examples from each major group confirmed changes seen by array, with an intermediate level in 5HTT+/- mice. Conclusions: These results for the first time show the in vivo effects of 5HTT knockout in lungs, and show that many of the downstream mechanisms suggested by cell culture and ex vivo experiments are also operational in vivo.  This suggests that the effect of 5HTT on pulmonary vascular function arises from its impact on several systems, including vasoreactivity, proliferation, and immune function."
GSE11035_series_matrix.txtimp_info.txt
5-HTT r is 6 
Found -/- in !Series_summary	"Rationale: While modulation of the serotonin transporter (5HTT) has shown to be a risk factor for pulmonary arterial hypertension for almost 40 years, there is a lack of in vivo data about the broad molecular effects of pulmonary inhibition of 5HTT. Previous studies have suggested effects on inflammation, proliferation, and vasoconstriction. The goal of this study was to determine which of these were supported by alterations in gene expression in serotonin transporter knockout mice. Methods: Eight week old normoxic mice with a 5-HTT knock-out (5HTT-/-) and their heterozygote(5HTT+/-) or wild-type(5HTT+/+) littermates had right ventricular systolic pressure(RVSP) assessed, lungs collected for RNA, pooled, and used in duplicate in Affymetrix array analysis. Representative genes were confirmed by quantitative RT-PCR and western blot. Results: RVSP was normal in all groups. Only 124 genes were reliably changed between 5HTT-/- and 5HTT+/+ mice. More than half of these were either involved in inflammatory response or muscle function and organization; in addition, some matrix, heme oxygenase, developmental, and energy metabolism genes showed altered expression. Quantitative RT-PCR for examples from each major group confirmed changes seen by array, with an intermediate level in 5HTT+/- mice. Conclusions: These results for the first time show the in vivo effects of 5HTT knockout in lungs, and show that many of the downstream mechanisms suggested by cell culture and ex vivo experiments are also operational in vivo.  This suggests that the effect of 5HTT on pulmonary vascular function arises from its impact on several systems, including vasoreactivity, proliferation, and immune function."
GSE11053_series_matrix.txtimp_info.txt
Mxi1 r is 1 
Found deficient in !Series_title	"Confirmation of the gene expression pattern in Mxi1-deficient mouse"
GSE11053_series_matrix.txtimp_info.txt
Mxi1 r is 1 
Found KO in !Series_summary	"For final aim to completes network map between gene that is concerned in cystogenesis, verifies meaning genes connected with cyst formation analyzing gene pattern in Mxi1 KO mouse that have phenotype of polycystic kidney disease. Monitoring meaning genes through microarray analysis, and confirm the function of these genes. Also, find pathway including meaning genes and new pathway related with PKD. Completes network map concerned in cystogenesis through integrates knowing pathway and predicting pathway. Develope diagnostic of cyst disease and cure target through such completed network map, and wish to clear new role of cyst formation connection gene through in vivo model and examine closely control system of cyst formation mechanism. "
GSE11098-GPL1261_series_matrix.txtimp_info.txt
Fah r is 5 
Found knockout in !Series_overall_design	"Livers from adult wildtype, Fah or Fah, p21 knockout mice were analyzed either after continuous treatment (ON) with NTBC or after NTBC withdrawal for 14 days (OFF)."
GSE11098-GPL1261_series_matrix.txtimp_info.txt
p21 r is 1 
Found knockout in !Series_overall_design	"Livers from adult wildtype, Fah or Fah, p21 knockout mice were analyzed either after continuous treatment (ON) with NTBC or after NTBC withdrawal for 14 days (OFF)."
GSE11098-GPL339_series_matrix.txtimp_info.txt
Fah r is 5 
Found knockout in !Series_overall_design	"Livers from adult wildtype, Fah or Fah, p21 knockout mice were analyzed either after continuous treatment (ON) with NTBC or after NTBC withdrawal for 14 days (OFF)."
GSE11098-GPL339_series_matrix.txtimp_info.txt
p21 r is 1 
Found knockout in !Series_overall_design	"Livers from adult wildtype, Fah or Fah, p21 knockout mice were analyzed either after continuous treatment (ON) with NTBC or after NTBC withdrawal for 14 days (OFF)."
GSE11105_series_matrix.txtimp_info.txt
SOCS r is 2 
Found expressing in !Series_summary	"We generated transgenic mice expressing constitutively SOCS-3 specifically in skeletal muscle. SOCS proteins are implicated in the negative regulation of various pathways including insulin signaling pathway. Our transgenic mice are predisposed to obesity and systemic insulin resistance compared to control mice."
GSE11116_series_matrix.txtimp_info.txt
Atf4 r is 1 
Found knockout in !Series_overall_design	"The low expressing Ttr::Fv2E-Perk transgene (#58) was bred into the Atf4 knockout strain and the derivative compound heterozygous mice (in the mixed FvB/n; Swiss Webster background) were backcrossed to the Atf4+/- parental stock and Ttr::Fv2E-PERK positive siblings with Atf4+/+ and  Atf4-/- genetypes were analyzed."
GSE11116_series_matrix.txtimp_info.txt
Atf4 r is 1 
Found -/- in !Series_title	"ISR target genes in the liver of mock-injected and AP20187-treated mice of wildtype and Atf4-/- genotype"
GSE11116_series_matrix.txtimp_info.txt
Atf4 r is 5 
Found treated in !Series_title	"ISR target genes in the liver of mock-injected and AP20187-treated mice of wildtype and Atf4-/- genotype"
GSE11116_series_matrix.txtimp_info.txt
Perk r is 2 
Found expressing in !Series_overall_design	"The low expressing Ttr::Fv2E-Perk transgene (#58) was bred into the Atf4 knockout strain and the derivative compound heterozygous mice (in the mixed FvB/n; Swiss Webster background) were backcrossed to the Atf4+/- parental stock and Ttr::Fv2E-PERK positive siblings with Atf4+/+ and  Atf4-/- genetypes were analyzed."
GSE11139_series_matrix.txtimp_info.txt
Hdh r is 8 
Found deletion in !Series_summary	"The polyglutamine expansion in huntingtin (Htt) protein is a cause of Huntington’s disease (HD).  Htt is an essential gene as  deletion of the mouse Htt gene homolog (Hdh) is embryonic lethal in mice. Therefore, in addition to elucidating the mechanisms responsible for polyQ-mediated pathology, it is also important to understand the normal function of Htt protein for both basic biology and for HD. To systematically search for a mouse Htt function, we took advantage of the Hdh +/- and Hdh-floxed mice and generated four mouse embryonic fibroblast (MEF) cells lines which contain a single copy of the Hdh gene (Hdh-HET) and four MEF lines in which the Hdh gene was deleted (Hdh-KO).   The function of Htt in calcium (Ca2+) signaling was analyzed in Ca2+ imaging experiments with generated cell lines.   We found that the cytoplasmic Ca2+ spikes resulting from the activation of inositol 1,4,5-trisphosphate receptor (InsP3R) and the ensuing mitochondrial Ca2+ signals were suppressed in the Hdh-KO cells when compared to Hdh-HET cells.  Furthermore,  in experiments with permeabilized cells we found that the InsP3-sensitivity of Ca2+ mobilization from endoplasmic reticulum was reduced in Hdh-KO cells.  These results indicated that Htt plays an important role in modulating InsP3R-mediated Ca2+ signaling.  To further evaluate function of Htt, we performed genome-wide transcription profiling of generated  Hdh-HET and Hdh-KO cells by microarray.  Our results revealed that 106 unique transcripts were downregulated by more than two-fold with p < 0.05 and 173 unique transcripts were upregulated at least two-fold with p < 0.05 in Hdh-KO cells when compared to Hdh-HET cells.  The microarray results were confirmed by quantitative real-time PCR for a number of affected transcripts.  Several signaling pathways affected by Hdh gene deletion were identified from annotation of the microarray results.   The unbiased approach used in our study provides novel and unique information about the normal function of Htt in cells, which may contribute to our understanding and treatment of HD."
GSE11139_series_matrix.txtimp_info.txt
huntingtin r is 5 
Found null in !Series_title	"Elucidating a normal function of huntingtin by analysis of huntingtin-null mouse embryonic fibroblasts"
GSE11139_series_matrix.txtimp_info.txt
Hdh r is 8 
Found KO in !Series_overall_design	"we generate four Hdh-HET MEF cell lines and four Hdh-KO MEF cell lines, and performed genome-wide transcription profiling of generated  Hdh-HET and Hdh-KO cells by microarray."
GSE11139_series_matrix.txtimp_info.txt
HET r is 7 
Found KO in !Series_overall_design	"we generate four Hdh-HET MEF cell lines and four Hdh-KO MEF cell lines, and performed genome-wide transcription profiling of generated  Hdh-HET and Hdh-KO cells by microarray."
GSE11139_series_matrix.txtimp_info.txt
InsP3R r is 7 
Found activation in !Series_summary	"The polyglutamine expansion in huntingtin (Htt) protein is a cause of Huntington’s disease (HD).  Htt is an essential gene as  deletion of the mouse Htt gene homolog (Hdh) is embryonic lethal in mice. Therefore, in addition to elucidating the mechanisms responsible for polyQ-mediated pathology, it is also important to understand the normal function of Htt protein for both basic biology and for HD. To systematically search for a mouse Htt function, we took advantage of the Hdh +/- and Hdh-floxed mice and generated four mouse embryonic fibroblast (MEF) cells lines which contain a single copy of the Hdh gene (Hdh-HET) and four MEF lines in which the Hdh gene was deleted (Hdh-KO).   The function of Htt in calcium (Ca2+) signaling was analyzed in Ca2+ imaging experiments with generated cell lines.   We found that the cytoplasmic Ca2+ spikes resulting from the activation of inositol 1,4,5-trisphosphate receptor (InsP3R) and the ensuing mitochondrial Ca2+ signals were suppressed in the Hdh-KO cells when compared to Hdh-HET cells.  Furthermore,  in experiments with permeabilized cells we found that the InsP3-sensitivity of Ca2+ mobilization from endoplasmic reticulum was reduced in Hdh-KO cells.  These results indicated that Htt plays an important role in modulating InsP3R-mediated Ca2+ signaling.  To further evaluate function of Htt, we performed genome-wide transcription profiling of generated  Hdh-HET and Hdh-KO cells by microarray.  Our results revealed that 106 unique transcripts were downregulated by more than two-fold with p < 0.05 and 173 unique transcripts were upregulated at least two-fold with p < 0.05 in Hdh-KO cells when compared to Hdh-HET cells.  The microarray results were confirmed by quantitative real-time PCR for a number of affected transcripts.  Several signaling pathways affected by Hdh gene deletion were identified from annotation of the microarray results.   The unbiased approach used in our study provides novel and unique information about the normal function of Htt in cells, which may contribute to our understanding and treatment of HD."
GSE11141_series_matrix.txtimp_info.txt
NgR r is 8 
Found treated in !Series_summary	"1) Bitransgenic +  water (through entire lifespan): The animals in this group were never treated with doxycycline, and therefore expressed the NgR transgene upon activity of the CamKII promoter."
GSE11141_series_matrix.txtimp_info.txt
NgR r is 1 
Found overexpression in !Series_title	"Effects of NgR overexpression on the developing and mature forebrain (backm-affy-mouse-433094)"
GSE11141_series_matrix.txtimp_info.txt
NgR r is 1 
Found overexpression in !Series_summary	"- Effects of NgR overexpression in the mature forebrain -"
GSE11141_series_matrix.txtimp_info.txt
NgR r is 1 
Found overexpression in !Series_summary	"- Effects of NgR overexpression in the developing forebrain  -"
GSE11141_series_matrix.txtimp_info.txt
NgR r is 1 
Found overexpression in !Series_summary	"We will also analyze the effects of NgR overexpression in bitransgenic animals raised on water.  In these animals, the NgR transgene is expressed in the forebrain upon activation of the CamKII promoter.  Since neuronal differentiation and neuronal pathways are being formed during development, we anticipate that NgR overexpression (de)effects in these animals will be markedly different to those observed in adult animals."
GSE11141_series_matrix.txtimp_info.txt
NgR r is 3 
Found + in !Series_summary	"1)  Experimental group: Bitrasgenic + water: Overexpresses NgR in forebrain neurons. In this group, doxyxycline was removed from the drinking water in adult animals. All the control groups were aged matched."
GSE11149_series_matrix.txtimp_info.txt
NCC r is 2 
Found deficient in !Series_summary	"FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development."
GSE11149_series_matrix.txtimp_info.txt
FAK r is 1 
Found knockout in !Series_summary	"1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis."
GSE11149_series_matrix.txtimp_info.txt
NCC r is 3 
Found knockout in !Series_summary	"1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis."
GSE11149_series_matrix.txtimp_info.txt
FAK r is 6 
Found deletion in !Series_summary	"Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development."
GSE11161_series_matrix.txtimp_info.txt
SMGA r is 7 
Found expressing in !Series_overall_design	"Bladder cells were FACS sorted from newborn double transgenic mice expressing EGFP under the control of a SMGA promoter and EYFP under the control of a SMAA promoter. Total RNA was isolated and underwent 2-round amplification (Epicentre® Biotechnologies) for gene expression analysis using the Affymetrix MOE430 microarray chip."
GSE11178_series_matrix.txtimp_info.txt
Fbw7 r is 1 
Found deficient in !Series_overall_design	"Four samples were analyzed: wild-type (WT) control and Fbw7-deficient (FBW7) Lin-ckit+Sca1+ (LSK) cells, as well as Lin-ckit+Sca1- myeloid progenitor (MP) cells, which served as a control for LSK-enriched/specific genes.  Total bone marrow cells were pooled from three WT and three FBW7 mice before sorting LSK and MP populations."
GSE11178_series_matrix.txtimp_info.txt
cyclin r is 8 
Found knock-out in !Series_summary	"Ubiquitination is a post-translational mechanism of control of diverse cellular processes. We focus here on the ubiquitin ligase Fbw7, a recently identified hematopoietic tumor suppressor that can target for degradation several important oncogenes including Notch1, c-Myc and cyclin E. We have generated conditional Fbw7 knock-out animals and inactivated the gene in hematopoietic stem cells (HSC) and their differentiated progeny. Deletion of Fbw7 specifically and rapidly affects the HSC compartment in a cell-autonomous manner. Fbw7-/- HSCs show defective maintenance of quiescence, leading to impaired self-renewal and a severe loss of competitive repopulating capacity. Furthermore, Fbw7-/- HSC  are unable to colonize the thymus leading to a profound depletion of T cell progenitors. Deletion of Fbw7 in bone marrow stem cells and progenitors leads to the stabilization of c-Myc, a transcription factor previously implicated in HSC self-renewal. On the other hand, neither Notch1 nor cyclin E are stabilized in the bone marrow of Fbw7 deficient mice. Genome-wide transcriptome studies of Fbw7-/- HSC and hematopoietic progenitors indicate that Fbw7 controls, through the regulation of HSC cell cycle entry, the global transcriptional “signature” that is associated with the quiescent, self-renewing HSC phenotype."
GSE11186_series_matrix.txtimp_info.txt
Bmal1 r is 1 
Found mutant in !Series_summary	"Hair follicles undergo recurrent cycling of controlled growth (anagen), regression (catagen), and relative quiescence (telogen) with a defined periodicity. Taking a genomics approach to study gene expression during synchronized mouse hair follicle cycling, we discovered that, in addition to circadian fluctuation, CLOCK-regulated genes are also modulated in phase with the hair growth cycle. During telogen and early anagen, circadian clock genes are prominently expressed in the secondary hair germ, which contains precursor cells for the growing follicle. Analysis of Clock and Bmal1 mutant mice reveals a delay in anagen progression, and the secondary hair germ cells show decreased levels of phosphorylated Rb and lack mitotic cells, suggesting that circadian clock genes regulate anagen progression via their effect on the cell cycle. Consistent with a block at the G1 phase of the cell cycle, we show a significant upregulation of p21 in Bmal1 mutant skin. While circadian clock mechanisms have been implicated in a variety of diurnal biological processes, our findings indicate that circadian clock genes may be utilized to modulate the progression of non-diurnal cyclic processes."
GSE11197_series_matrix.txtimp_info.txt
miR-146a r is 7 
Found treated in !Series_summary	"microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system.  Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity.  In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice.  We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls.  Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes.  Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes.  miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. "
GSE11197_series_matrix.txtimp_info.txt
miR-223 r is 7 
Found treated in !Series_summary	"microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system.  Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity.  In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice.  We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls.  Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes.  Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes.  miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. "
GSE11197_series_matrix.txtimp_info.txt
E2 r is 8 
Found induced in !Series_title	"Suppression of LPS-induced IFNg and NO in splenocytes by select E2-regulated miRNA: A novel mechanism of immune mod."
GSE11197_series_matrix.txtimp_info.txt
iNOS r is 8 
Found induced in !Series_summary	"microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system.  Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity.  In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice.  We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls.  Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes.  Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes.  miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. "
GSE11197_series_matrix.txtimp_info.txt
inducible nitric oxide synthase r is 3 
Found induced in !Series_summary	"microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system.  Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity.  In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice.  We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls.  Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes.  Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes.  miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. "
GSE11210_series_matrix.txtimp_info.txt
Atf4 r is 1 
Found knockout in !Series_overall_design	"bred into the Atf4 knockout strain and the derivative compound heterozygous mice (in the mixed FvB/n; Swiss Webster background) were backcrossed to the Atf4+/- parental stock and Ttr::Fv2E-PERK positive siblings with Atf4+/+ and  Atf4-/- genetypes were analyzed."
GSE11210_series_matrix.txtimp_info.txt
Perk r is 2 
Found expressing in !Series_overall_design	"The high expressing Ttr::Fv2E-Perk transgenic mice was injected by either mock or AP20187. Wildtype and Alb::GC transgenic mice were fed by either Low Fat Diet (LFD) or High Fat Diet (HFD) ."
GSE11226_series_matrix.txtimp_info.txt
Nkx2-1 r is 2 
Found null in !Series_overall_design	"DNA microarray was performed using RNAs isolated from 4 day-organ cultured Nkx2-1-null lungs with and without SCGB3A2 treatment."
GSE11229_series_matrix.txtimp_info.txt
Dicer1 r is 1 
Found deficient in !Series_summary	"We identify the miR-290 cluster as being downregulated in Dicer1-deficient cells and show that it silences Rbl2, thereby controlling Dnmt expression. These results identify a pathway by which miR-290 directly regulates Rbl2-dependent Dnmt expression, indirectly affecting telomere-length homeostasis."
GSE11229_series_matrix.txtimp_info.txt
Rbl2 r is 7 
Found deficient in !Series_summary	"We identify the miR-290 cluster as being downregulated in Dicer1-deficient cells and show that it silences Rbl2, thereby controlling Dnmt expression. These results identify a pathway by which miR-290 directly regulates Rbl2-dependent Dnmt expression, indirectly affecting telomere-length homeostasis."
GSE11229_series_matrix.txtimp_info.txt
retinoblastoma-like 2 r is 5 
Found overexpression in !Series_summary	"Dicer initiates RNA interference by generating small RNAs involved in various silencing pathways. Dicer participates in centromeric silencing, but its role in the epigenetic regulation of other chromatin domains has not been explored. Here we show that Dicer1 deficiency in Mus musculus leads to decreased DNA methylation, concomitant with increased telomere recombination and telomere elongation. These DNA-methylation defects correlate with decreased expression of Dnmt1, Dnmt3a and Dnmt3b DNA methyltransferases (Dnmts), and methylation levels can be recovered by their overexpression. We identify the retinoblastoma-like 2 protein (Rbl2) as responsible for decreased Dnmt expression in Dicer1-null cells, suggesting the existence of Dicer-dependent small RNAs that target Rbl2."
GSE11229_series_matrix.txtimp_info.txt
Dnmt1 r is 1 
Found overexpressing in !Series_title	"Dicer-null cell lines vs. wt ES cells and Dicer-null cell lines vs. Dicer-null cells overexpressing Dnmt1 or Dnmt3a/3b"
GSE11252_series_matrix.txtimp_info.txt
Aag r is 2 
Found null in !Series_summary	"We are investigating the transcriptional response of mice that are wt or null for Aag in response to alkylating agent MMS"
GSE11252_series_matrix.txtimp_info.txt
Aag r is 1 
Found null in !Series_overall_design	"Mice (WT and Aag null) were treated with MMS and livers extracted at 6, 12, 24, and 48 hours"
GSE11252_series_matrix.txtimp_info.txt
Aag r is 4 
Found treated in !Series_overall_design	"Mice (WT and Aag null) were treated with MMS and livers extracted at 6, 12, 24, and 48 hours"
GSE11253_series_matrix.txtimp_info.txt
p130 r is 4 
Found deficient in !Series_title	"Expression data from Rb family (Rb, p130 and p107) deficient Hematopoietic stem Cells"
GSE11253_series_matrix.txtimp_info.txt
p107 r is 2 
Found deficient in !Series_title	"Expression data from Rb family (Rb, p130 and p107) deficient Hematopoietic stem Cells"
GSE11253_series_matrix.txtimp_info.txt
Rb r is 2 
Found deficient in !Series_summary	"Keywords: unpaired WT versus Rb family deficient KLS"
GSE11253_series_matrix.txtimp_info.txt
Rb r is 4 
Found induced in !Series_overall_design	"We used mice that harbor floxed alleles for the Rb family and we induced the recombination by 6 weeks of age. KLS (c-Kit+ Lin - Sca-1+) cells were sorted 2 months after the recombination."
GSE11258_series_matrix.txtimp_info.txt
Npas4 r is 1 
Found expressing in !Series_overall_design	"We infected mouse hippocampal neurons with lentivirus expressing Npas4-RNAi or control-RNAi @ 3 DIV and depolarized the neurons @ 8 DIV with 50 mM of KCl for 0, 1, 3 or 6 hours. Neurons were lysed, mRNA isolated and hybridized to Affymetrix arrays. Data were collected from 3 independent experiments."
GSE11276_series_matrix.txtimp_info.txt
Nogo-A r is 2 
Found KO in !Series_title	"Comparison of adult intact naive C57Bl/6 Nogo-A KO versus WT spinal cord"
GSE11276_series_matrix.txtimp_info.txt
Nogo-A r is 2 
Found KO in !Series_summary	"Nogo-A localized on myelin adaxonal membrane in the adult CNS is well known for its role as neurite outgrowth inhibitor following a lesion. Nogo-A KO mice show enhanced regenerative/compensatory fiber growth following CNS lesion. However, changes undergoing in their intact CNS have not been studied. Moreover, Nogo-A in the intact adult CNS in also expressed in some neuronal subpopulations, e.g. in the hippocampus, olfactory bulbs and dorsal root ganglia."
GSE11276_series_matrix.txtimp_info.txt
Nogo-A r is 2 
Found KO in !Series_summary	"We compared the intact adult CNS (spinal cord) of Nogo-A KO mice in order to identify: potential compensating molecules which could be interesting new inhibitory neurite outgrowth candidates, possible molecules involved in the up to now not yet clarified downstream signalling pathway of Nogo-A, additional new functions for myelin or neuronal Nogo-A in the intact adult CNS."
GSE11276_series_matrix.txtimp_info.txt
Nogo-A r is 2 
Found KO in !Series_summary	"Keywords: gene expression, Nogo-A KO, spinal cord, adult, naive, unlesioned"
GSE11276_series_matrix.txtimp_info.txt
Nogo-A r is 2 
Found KO in !Series_overall_design	"Spinal cords from 3 adult C57Bl/6 wild type and Nogo-A KO mice have been explanted. Total RNA has been extracted and processed for hybridization on Mouse 430 2.0 Affymetrix GeneChips. Following scanning and first analysis with MAS 5.0, further analysis was performed by GeneSpring 7.2 (Silicon Genetics, Redwood City, CA). A present call filter (2 out of 3 present calls in at least one out of the different studied conditions) was applied. Normalization was run per chip as well as per gene to the median of the control replicates. Data were statistical restricted through a 1-way Anova (p=0.05). A final threshold of =1.2 folds of increase or decrease in the expression level of each single transcript was applied. Regulated transcripts have been assigned to functional categories according to GeneOntology as well as literature and database mining (Pubmed and Bioinformatics Harvester EMBL Heidelberg)."
GSE11286_series_matrix.txtimp_info.txt
Apoe r is 5 
Found deficient in !Series_summary	"Mice deficient in Apolipoprotein E (Apoe E(-/-)) vs wild type mice were exposed to diesel engine particulate by single dose intratracheal instillation.  The transcript-level response of the hearts after 24h  and of the  lungs after 24 h and 5 days were subsequently analyzed by the 2-color microarray method."
GSE11286_series_matrix.txtimp_info.txt
Apo r is 3 
Found -/- in !Series_title	"Cardiac and pulmonary responses to diesel engine particulate in Apo E(-/-) mice"
GSE11286_series_matrix.txtimp_info.txt
Apoe r is 3 
Found -/- in !Series_summary	"Mice deficient in Apolipoprotein E (Apoe E(-/-)) vs wild type mice were exposed to diesel engine particulate by single dose intratracheal instillation.  The transcript-level response of the hearts after 24h  and of the  lungs after 24 h and 5 days were subsequently analyzed by the 2-color microarray method."
GSE11286_series_matrix.txtimp_info.txt
Apo r is 4 
Found -/- in !Series_overall_design	"Four mice of the Apo E (-/-) strain were exposed to diesel engine particulate from the National Institute of Standards and Technology via intratracheal instillation.  Controls consisted of 4 littermates exposed to saline vehicle.  Four wild type mice were similarly exposed to diesel particulate and four to vehicle control.  24 hours after exposure, mice were humanely sacrificed by carbon dioxide asphyxiation and the hearts and lungs were collected and frozen for analysis of total RNA.  2 color microarrays were utilized to compare pooled RNA representing all four animals of each strain, and  in each condition and in each tissue."
GSE11287_series_matrix.txtimp_info.txt
Keap1 r is 1 
Found knockout in !Series_title	"Keap1-dependent gene expression determined in the liver using conditional Keap1 knockout mice vs. genetic control mice"
GSE11287_series_matrix.txtimp_info.txt
Alb r is 2 
Found knockout in !Series_summary	"To compare hepatic gene expression in conditional Keap1 knockout (Alb-Cre:Keap1(flox/-)) and genetic control mice. Disruption of Keap1-mediated repression of Nrf2 signaling was expected to result in increased expression of Nrf2-regulated genes."
GSE11287_series_matrix.txtimp_info.txt
Keap1 r is 1 
Found knockout in !Series_summary	"To compare hepatic gene expression in conditional Keap1 knockout (Alb-Cre:Keap1(flox/-)) and genetic control mice. Disruption of Keap1-mediated repression of Nrf2 signaling was expected to result in increased expression of Nrf2-regulated genes."
GSE11287_series_matrix.txtimp_info.txt
Alb r is 6 
Found knockout in !Series_overall_design	"Hepatic gene expression was compared in conditional Keap1 knockout and genetic control mice (Alb-Cre:Keap1(flox/+)) mice.  Male 9 week old mice were used, n=3/group."
GSE11287_series_matrix.txtimp_info.txt
Keap1 r is 1 
Found knockout in !Series_overall_design	"Hepatic gene expression was compared in conditional Keap1 knockout and genetic control mice (Alb-Cre:Keap1(flox/+)) mice.  Male 9 week old mice were used, n=3/group."
GSE11317_series_matrix.txtimp_info.txt
progesterone receptor r is 4 
Found deficient in !Series_summary	"The lymphatic system is a common avenue for the spread of breast cancer cells and dissemination through it occurs at least as frequently as hematogenous metastasis. Approximately 75% of primary breast cancers are estrogen receptor (ER) positive and the majority of these maintain receptor expression as lymph node (LN) metastases. However, it is unknown if ER function is equivalent in cancer cells growing in the breast and in the LNs. We have developed a model to assess estrogen responsiveness in ER(+) breast tumors and LN metastases. Fluorescent ER(+) MCF-7 tumors were grown in ovariectomized nude mice supplemented with estradiol. Once axillary LN metastasis arose, estradiol was withdrawn (EWD), for 1 or 4 weeks, or continued, to assess estradiol responsiveness. On EWD, proliferation rates fell similarly in tumors and LN metastases. However, estradiol-dependent ER down-regulation and progesterone receptor induction were deficient in LN metastases, indicating that ER-dependent transcriptional function was altered in the LN. Cancer cells from estradiol-treated and EWD primary tumors and matched LN metastases were isolated by laser capture microdissection. Global gene expression profiling identified transcripts that were regulated by the tissue microenvironment, by hormones, or by both. Interestingly, numerous genes that were estradiol regulated in tumors lost estradiol sensitivity or were regulated in the opposite direction by estradiol in LN metastases. We propose that the LN microenvironment alters estradiol signaling and may contribute to local antiestrogen resistance."
GSE11321_series_matrix.txtimp_info.txt
p53 r is 2 
Found deletion in !Series_summary	"Neural tube defects (NTDs) are one of the most common human birth defects, with a prevalence of approximately 1 in 1000 live births in the United States.  In animal studies, deletion of p53 leads to a significant increase in embryos that exhibit exencephaly.  Whereas several studies have closely investigated the morphological changes of p53-deficient embryos, there is no study that has reported the molecular-level alternations in p53-deficient embryos.  Here we use microarray approach to find genes modified by deletion of p53 in day 8.5 mouse embryos to identify genes that may be involved in the mechanisms underlining NTDs and begin to define the developmental role of p53 in the etiology of NTDs.      "
GSE11322_series_matrix.txtimp_info.txt
Xbp1 r is 1 
Found knockout in !Series_summary	"XBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated.  Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons."
GSE11331_series_matrix.txtimp_info.txt
Rps6 r is 3 
Found deletion in !Series_title	"Ribosomal protein S6 Rps6 heterozygous null deletion effect on footpad epidermis"
GSE11331_series_matrix.txtimp_info.txt
Rps6 r is 2 
Found deletion in !Series_summary	"The tissue (footpad epidermis) is from a conditional heterozygous null deletion of Rps6. One copy of Rps6 was deleted from keratinocytes in the skin using the K5.Cre transgene."
GSE11331_series_matrix.txtimp_info.txt
Rps6 r is 2 
Found null in !Series_title	"Ribosomal protein S6 Rps6 heterozygous null deletion effect on footpad epidermis"
GSE11331_series_matrix.txtimp_info.txt
Rps6 r is 3 
Found null in !Series_summary	"The tissue (footpad epidermis) is from a conditional heterozygous null deletion of Rps6. One copy of Rps6 was deleted from keratinocytes in the skin using the K5.Cre transgene."
GSE11346_series_matrix.txtimp_info.txt
Apoe r is 1 
Found knockout in !Series_overall_design	"12-13 weeks old Apoe knockout mice (C57BL/6-Apoe tm1) mice were injected intraperitoneally with varying doses of SRM 2975. In a parallel experiment C57BL mice were exposed by inhalation for 90 minutes to four consecutive doses of 20mg/m3 of filtered air, NIST 2975 or Ptintex 90. Livers and aortic tissue were collected."
GSE11396_series_matrix.txtimp_info.txt
growth hormone receptor r is 1 
Found mutant in !Series_title	"Gene expression of transgenic knock-in mutant growth hormone receptor mice"
GSE11398-GPL81_series_matrix.txtimp_info.txt
LIF r is 7 
Found overexpressing in !Series_overall_design	"FVB/N derived embryonic stem cells cultivated in the presence of LIF were compared with FVB/N ES cells overexpressing STAT3-MER and cultivated in the presence of 4-hydroxytamoxifen and absence of LIF"
GSE11398-GPL82_series_matrix.txtimp_info.txt
LIF r is 7 
Found overexpressing in !Series_overall_design	"FVB/N derived embryonic stem cells cultivated in the presence of LIF were compared with FVB/N ES cells overexpressing STAT3-MER and cultivated in the presence of 4-hydroxytamoxifen and absence of LIF"
GSE11398-GPL83_series_matrix.txtimp_info.txt
LIF r is 7 
Found overexpressing in !Series_overall_design	"FVB/N derived embryonic stem cells cultivated in the presence of LIF were compared with FVB/N ES cells overexpressing STAT3-MER and cultivated in the presence of 4-hydroxytamoxifen and absence of LIF"
GSE11443_series_matrix.txtimp_info.txt
pl r is 7 
Found -/- in !Series_title	"Choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice (carri-affy-mouse-302760)"
GSE11443_series_matrix.txtimp_info.txt
PL r is 2 
Found -/- in !Series_title	"Choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice (carri-affy-mouse-302760)"
GSE11443_series_matrix.txtimp_info.txt
B10 r is 8 
Found -/- in !Series_title	"Choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice (carri-affy-mouse-302760)"
GSE11443_series_matrix.txtimp_info.txt
pl r is 7 
Found -/- in !Series_summary	"Previous work has led us to examine the differences in the choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice. We believe that there is a difference between those that are normal functioning and those that are lymphocyte deficient."
GSE11443_series_matrix.txtimp_info.txt
PL r is 2 
Found -/- in !Series_summary	"Previous work has led us to examine the differences in the choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice. We believe that there is a difference between those that are normal functioning and those that are lymphocyte deficient."
GSE11443_series_matrix.txtimp_info.txt
B10 r is 8 
Found -/- in !Series_summary	"Previous work has led us to examine the differences in the choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice. We believe that there is a difference between those that are normal functioning and those that are lymphocyte deficient."
GSE11494_series_matrix.txtimp_info.txt
M1 r is 2 
Found deletion in !Series_overall_design	"C57BL/6 mice (6-10 weeks old), 4 per group, were infected intranasally with log-phase Streptococcus pyogenes, 2 to 4 x 10^8 CFU per 15 µl of pyrogen-free PBS.  Sham-infected mice were administered 15 µl of the same PBS.  Mice were infected with wild type strain 90-226 (Cue 1998), a 90-226 strain containing an in-frame deletion of M1 protein (90-226 delta emm1) (Zimmerlein 2005) or an attenuated 90-226 which lacks both M1 and SCPA proteins (90-226att).  NALT was collected from mice at 24h after infection and stored in RNAlater until RNA could be purified)."
GSE11496_series_matrix.txtimp_info.txt
Met r is 8 
Found -/- in !Series_overall_design	"Gcn2 wild-type or knockout mouse liver were perfused with complete amino acids media or media lacking methionine for RNA extraction and hybridization of Affymetrix microarrays.  RNA was extracted from unfractionated liver samples and polysome fraction of samples separated on sucrose density gradient.  To minimize biological variations, we pooled RNA from two perfused liver samples to use in each array analysis.  The conditions were total and polysome fraction of Gcn2+/+, +Met or -Met; total and polysome fraction of Gcn2-/-, +Met or -Met.  Each array analysis was done in duplicate."
GSE11496_series_matrix.txtimp_info.txt
GCN2 r is 2 
Found activation in !Series_summary	"We use array analysis to determine the global mRNA shift into polysomes following a stress response, and to compare the translational response following activation of GCN2 versus PERK, two of the four eIF2alpha kinases."
GSE11498_series_matrix.txtimp_info.txt
Irg1 r is 7 
Found induced in !Series_summary	"Results. Eleven of the 12 most highly upregulated mRNAs related to innate immunity and inflammation. They included mRNAs encoding histidine decarboxylase (the enzyme that synthesizes histamine), interleukin (IL)-6, the cell surface receptors PUMA-g and TREM-1, and the polypeptides Irg1 and PROK-2. MSU crystals induced dramatic rises in these mRNAs in the pouch membrane within 3-8 hours after the surge in pro-inflammatory cytokine (IL-6, IL-1beta and TNFalpha) and immediate early gene (Egr-1) transcription, which occurred 1h after crystal injection. MSU crystals induced these mRNAs in cultured macrophages with similar kinetics but lower fold changes. In keeping with their downregulation by MSU crystals according to the microarrays, qPCR confirmed that TREM-2 and granzyme D mRNAs decreased 79% and 94%, respectively, in MSU crystal inflamed membranes."
GSE11507_series_matrix.txtimp_info.txt
Abcb4 r is 3 
Found -/- in !Series_summary	"Background. Abcb4 (-/-) mice secrete phosphatidylcholine-deficient bile and develop sclerosing cholangitis (SC). The cholangitis involves differential hepatic transcription of genes whose products govern inflammation, activation of hepatic stellate cells and fibrosis.  This study was undertaken to test the hypothesis that several genes involved in regulation of tissue inflammation and fibrosis display transcription rates that reflect SC disease activity. Methods. Abcb4 (-/-) mice fed cholic acid (CA) display high SC activity and ursodeoxycholic acid (UDCA) fed mice display low SC activity. Differential hepatic transcription of genes was accordingly measured in abcb4 (-/-) mice maintained on CA- and UDCA-supplemented diets using cDNA microarrays. Abcb4 (+/+) mice served as controls. The differential transcription of selected genes was verified by real time polymerase chain reaction. Liver tissue pathology was quantified by histopathology scoring and immunohistochemistry to visualize bile duct cells and activated hepatic stellate cells. Results. Differential transcription of  Ccl2, Ccl20, Cxcl10, Nfκb1, Nfκb2, Tgfβ1, Tgfβ2, Sparc, Ctgf, Lgals3, Elf3, Spp1, Pdgfa, Pdgfrb, Col1a1, Col1a2 and Col4a1 genes paralleled the differing SC activities of cholic acid- and UDCA-fed abcb4 (-/-) mice. Histopathology scores and immunohistochemistry showed greatly enhanced activation of hepatic stellate cells during high SC activity due to CA feeding. Conclusion. Differential transcription of several genes relating to tissue inflammation and hepatic stellate cell activation parallels SC activity in abcb4 (-/-) mice. Data on their differential transcription may be used to gauge SC disease activity. "
GSE11547_series_matrix.txtimp_info.txt
p53 r is 2 
Found deletion in !Series_summary	"Neural tube defects (NTDs) are one of the most common human birth defects, with a prevalence of approximately 1 in 1000 live births in the United States. In animal studies, deletion of p53 and hyperthermia leads to a significant increase in embryos that exhibit exencephaly. To evaluate the effects of hyperthermia on p53-deficient mouse embryos we used microarray approach to find genes modified by deletion of p53 and hyperthermia treatment in day 8.5 mouse embryos to identify genes that may be involved in the mechanisms underlining NTDs and begin to define the developmental role of p53 in the etiology of NTDs. "
GSE11547_series_matrix.txtimp_info.txt
p53 r is 4 
Found treated in !Series_overall_design	"After day 8.5 mouse embryos from p53 heterozygous crosses were treated in either control (38C) water bath or hot (43C) water bath for 10 minutes, they were collected, genotyped, and embryos of similar genotype (+/+; +/-; -/-) and treatment were pooled. Total RNA of biological quarduplicate samples were isolated each from p53 +/+, +/-, -/- embryos. Total RNA of each sample was obtained from 3-7 embryos. Gene expression differences between the three genotypes were examined."
GSE11557_series_matrix.txtimp_info.txt
Evi-1 r is 2 
Found deletion in !Series_title	"Effect of Evi-1 deletion in hematopoietic stem cells"
GSE11557_series_matrix.txtimp_info.txt
Kit r is 4 
Found + in !Series_overall_design	"Lineage(-), Sca-1(+), c-Kit(+) cells derived from Evi-1(flox/flox) mice were transduced with GFP or Cre-GFP expressing retroviruses. GFP(+) cells were sorted and  and analyzed by Affymetrix® Mouse Genome 430 2.0 Array® for gene expression. Two independent experiments were performed."
GSE11557_series_matrix.txtimp_info.txt
Sca-1 r is 2 
Found + in !Series_overall_design	"Lineage(-), Sca-1(+), c-Kit(+) cells derived from Evi-1(flox/flox) mice were transduced with GFP or Cre-GFP expressing retroviruses. GFP(+) cells were sorted and  and analyzed by Affymetrix® Mouse Genome 430 2.0 Array® for gene expression. Two independent experiments were performed."
GSE11572_series_matrix.txtimp_info.txt
FU r is 1 
Found treated in !Series_overall_design	"BM cells from 5-FU treated mice were infected with viral constructs, sorted for GFP expression (day8), plated in IMDM , 10% FCS, 2mM Gln, 1% P/S, supplemented with 50ng/ml rSCF, 100ng/ml TPO and 100ng/ml G-CSF and cultured for 72h (day8-day10). On day10 cells were stimulated with 4-OHT (1uM) for 16h. After that time, total RNA was isolated by Trizol method."
GSE11585_series_matrix.txtimp_info.txt
ERbeta r is 4 
Found null in !Series_title	"Granulosa cell gene expression in gonadotropin-treated ERbeta-het and ERbeta-null mice"
GSE11585_series_matrix.txtimp_info.txt
het r is 3 
Found null in !Series_title	"Granulosa cell gene expression in gonadotropin-treated ERbeta-het and ERbeta-null mice"
GSE11585_series_matrix.txtimp_info.txt
het r is 3 
Found null in !Series_summary	"The aim of this study was to determine the role of ERβ in the response of mouse granulosa cells to PMSG (an FSH analog) by comparing the gene expression profiles of ERβ-het and ERβ-null animals treated with this compound."
GSE11585_series_matrix.txtimp_info.txt
het r is 3 
Found null in !Series_overall_design	"ERβ-het and ERβ-null mice were treated with PMSG for 48h and granulosa cells isolated and pooled according to gentoype, resulting in the production of two RNA samples (one biological replicate per gentoype). There were two hyb replicates for the comparison. Two slides were hybridized for the sample pairing to allow for dye reversals (technical replicates)."
GSE11585_series_matrix.txtimp_info.txt
ERbeta r is 1 
Found treated in !Series_title	"Granulosa cell gene expression in gonadotropin-treated ERbeta-het and ERbeta-null mice"
GSE11585_series_matrix.txtimp_info.txt
het r is 2 
Found treated in !Series_title	"Granulosa cell gene expression in gonadotropin-treated ERbeta-het and ERbeta-null mice"
GSE11585_series_matrix.txtimp_info.txt
het r is 5 
Found treated in !Series_summary	"The aim of this study was to determine the role of ERβ in the response of mouse granulosa cells to PMSG (an FSH analog) by comparing the gene expression profiles of ERβ-het and ERβ-null animals treated with this compound."
GSE11585_series_matrix.txtimp_info.txt
het r is 6 
Found treated in !Series_overall_design	"ERβ-het and ERβ-null mice were treated with PMSG for 48h and granulosa cells isolated and pooled according to gentoype, resulting in the production of two RNA samples (one biological replicate per gentoype). There were two hyb replicates for the comparison. Two slides were hybridized for the sample pairing to allow for dye reversals (technical replicates)."
GSE11591_series_matrix.txtimp_info.txt
Lrg r is 3 
Found deficient in !Series_summary	"To assess gene expression changes in Irgm1 (Lrg-47) deficient HSCs"
GSE11591_series_matrix.txtimp_info.txt
Irgm1 r is 5 
Found deficient in !Series_summary	"To assess gene expression changes in Irgm1 (Lrg-47) deficient HSCs"
GSE11591_series_matrix.txtimp_info.txt
Lrg r is 3 
Found -/- in !Series_title	"Expression profiling of Irgm1-/- (Lrg-47) HSCs"
GSE11591_series_matrix.txtimp_info.txt
Irgm1 r is 1 
Found -/- in !Series_title	"Expression profiling of Irgm1-/- (Lrg-47) HSCs"
GSE11596_series_matrix.txtimp_info.txt
Mecp2 r is 1 
Found null in !Series_title	"Gene expression profiles of wild type and Mecp2-null mice in three different regions of the brain"
GSE11596_series_matrix.txtimp_info.txt
Mecp2 r is 1 
Found null in !Series_overall_design	"Comparative experiment: Mecp2-null (KO) mice vs. their corresponding age-mated wild type (WT) littermates (CONTROLS). Four couples of KO-WT animals are used and three different brain regions are studied from each couple; cortex, midbrain, and cerebellum."
GSE11596_series_matrix.txtimp_info.txt
Mecp2 r is 3 
Found KO in !Series_overall_design	"Comparative experiment: Mecp2-null (KO) mice vs. their corresponding age-mated wild type (WT) littermates (CONTROLS). Four couples of KO-WT animals are used and three different brain regions are studied from each couple; cortex, midbrain, and cerebellum."
GSE11628_series_matrix.txtimp_info.txt
LIF r is 2 
Found treated in !Series_summary	"The molecular processes underlying the properties of ESC are yet unknown even when it's well established that LIF/STAT3 is neccesary for the maintenance of pluripotency. Other pathways as Wnt are may be implicated in the regulation of the biological mechanisms in mESC. Work model: D3-ES cultivated with or without LIF and treated with chronic (7 days) low doses (50nM) of GSK3 β inhibitor (lithium)."
GSE11628_series_matrix.txtimp_info.txt
D3 r is 8 
Found treated in !Series_summary	"The molecular processes underlying the properties of ESC are yet unknown even when it's well established that LIF/STAT3 is neccesary for the maintenance of pluripotency. Other pathways as Wnt are may be implicated in the regulation of the biological mechanisms in mESC. Work model: D3-ES cultivated with or without LIF and treated with chronic (7 days) low doses (50nM) of GSK3 β inhibitor (lithium)."
GSE11631_series_matrix.txtimp_info.txt
PU.1 r is 3 
Found null in !Series_summary	"Spermatogenesis in a null mutant (PU.1(G/G)) was arrested at the prenatal stage, with reduced numbers of gonocytes owing to a defect in proliferation already noticeable at E12.5. Transcripts of several germinal markers, including vasa (Mvh, Ddx4), Oct4 (Pou5f1), Dazl and Taf4b, were detected, whereas stella (PGC7, Dppa3) was not. Germ cells of PU.1(G/G) newborn testes grafted in nude mice did not initiate the postnatal replicative stage, whereas grafts of their wild-type littermates underwent complete spermatogenesis. During embryonic development, PU.1 transcription was initiated as early as the blastocyst stage, with a generalized expression at E6.5 in the embryonic ectoderm. PU.1 therefore appears to play a determinant role in at least two distinct lineages and, given its wide range of expression, possibly in other stem cells."
GSE11631_series_matrix.txtimp_info.txt
PU.1 r is 2 
Found mutant in !Series_summary	"Spermatogenesis in a null mutant (PU.1(G/G)) was arrested at the prenatal stage, with reduced numbers of gonocytes owing to a defect in proliferation already noticeable at E12.5. Transcripts of several germinal markers, including vasa (Mvh, Ddx4), Oct4 (Pou5f1), Dazl and Taf4b, were detected, whereas stella (PGC7, Dppa3) was not. Germ cells of PU.1(G/G) newborn testes grafted in nude mice did not initiate the postnatal replicative stage, whereas grafts of their wild-type littermates underwent complete spermatogenesis. During embryonic development, PU.1 transcription was initiated as early as the blastocyst stage, with a generalized expression at E6.5 in the embryonic ectoderm. PU.1 therefore appears to play a determinant role in at least two distinct lineages and, given its wide range of expression, possibly in other stem cells."
GSE11632_series_matrix.txtimp_info.txt
Tmprss6 r is 1 
Found deficient in !Series_title	"Transcriptional profiling of Tmprss6-deficient mouse liver"
GSE11660_series_matrix.txtimp_info.txt
Oct3/4 r is 3 
Found treated in !Series_summary	"Bone marrow stromal cells (BMSCs) are multipotent stem cells that preferentially differentiate into mesenchymal cells. If they can be dedifferentiated into embryonic stem cell-like cells, they will be a highly attractive source for cell therapy. Cell and egg extracts have been used in a few studies to evaluate nuclear reprogramming, but these have not examined cell pluripotency in any detail. In this study, we used a cell reversible permeabilization method to treat BMSC with Xenopus laevis mitotic egg extract. We observed an upregulation of the pluripotent protein Oct3/4 in BMSCs treated by this extract. We also further evaluated transcriptional changes with a focused stem cell oligonucleotide array. A number of genes involved in the Notch or Wnt signaling pathways were upregulated in BMSC exposed to Xenopus egg extract. In conclusion, our microarray data from BMSCs exposure to egg extracts may provide interesting clues regarding factors involved in nuclear reprogramming. Our approach is an alternative method towards dedifferentiation of cells without genetic modification, which is preferable in the clinical situation."
GSE11662_series_matrix.txtimp_info.txt
Akt r is 5 
Found induced in !Series_title	"GADD45a in ventilator-induced lung injury: role of Akt signaling"
GSE11662_series_matrix.txtimp_info.txt
Akt1 r is 5 
Found overexpression in !Series_summary	"We explored the mechanistic involvement of the growth arrest and DNA damageinducible gene, GADD45a, in LPS- and ventilator-induced inflammatory lung injury (VILI). Multiple biochemical and genomic parameters of inflammatory lung injury indicated GADD45a-/- mice to be modestly susceptible to intratracheal LPS-induced lung injury and profoundly susceptible to high tidal volume ventilation-induced lung injury (VILI) with increases in microvascular permeability and levels of inflammatory cytokines in bronchoalveolar lavage. Expression profiling of lung tissues from GADD45a-/- mice revealed strong dysregulation in the B cell receptor signaling pathway suggesting involvement of PI3 kinase/Akt signaling components while the wild type controls depicted no observable changes. Western blot analyses of lung homogenates confirmed ~50% reduction in Akt protein levels in GADD45a-/- mice accompanied by marked increases in Akt ubiquitination. Electrical resistance measurements across human lung endothelial cell monolayers with either reduced GADD45a or Akt expression (siRNAs) revealed significant potentiation of LPS-induced human lung endothelial barrier dysfunction which was attenuated by overexpression of a constitutively active Akt1 transgene. These studies validate GADD45a as a novel candidate gene in inflammatory lung injury and a significant participant in vascular barrier regulation via effects on Akt-mediated endothelial signaling"
GSE11674-GPL81_series_matrix.txtimp_info.txt
vascular endothelial cadherin r is 6 
Found inhibition in !Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."
GSE11674-GPL81_series_matrix.txtimp_info.txt
vascular endothelial cadherin r is 3 
Found induced in !Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."
GSE11674-GPL81_series_matrix.txtimp_info.txt
beta-catenin r is 7 
Found induced in !Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."
GSE11674-GPL82_series_matrix.txtimp_info.txt
vascular endothelial cadherin r is 6 
Found inhibition in !Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."
GSE11674-GPL82_series_matrix.txtimp_info.txt
vascular endothelial cadherin r is 3 
Found induced in !Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."
GSE11674-GPL82_series_matrix.txtimp_info.txt
beta-catenin r is 7 
Found induced in !Series_summary	"In order to identify genes regulated by VE-cadherin expression, we compared a mouse VE-cadherin null cell line (VEC null) with the same line reconstituted with VE-cadherin wild type cDNA (VEC positive). The morphological and functional properties of these cell lines were described previously [Lampugnani,M.G. et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J. Cell Biol. 161, 793-804 (2003)]. By Affymetrix gene expression analysis we found several genes up-regulated by VE-cadherin, among which claudin-5 reached remarkably high levels. The up-regulation of these genes required not only VE-cadherin expression but also cell confluence suggesting that VE-cadherin clustering at junctions was needed."
GSE11684_series_matrix.txtimp_info.txt
Perk r is 4 
Found knockout in !Series_title	"Expression data from Perk wild-type and knockout mouse liver perfused without or with 2,5-di-tert-butylhydroquinone"
GSE11684_series_matrix.txtimp_info.txt
Perk r is 1 
Found -/- in !Series_overall_design	"Perk wild-type or knockout mouse liver were perfused without or with 2,4-di-tert-butylhydroquinone (tBuHQ) for RNA extraction and hybridization of Affymetrix microarrays.  RNA was extracted from unfractionated liver samples and polysome fraction of samples separated on sucrose density gradient.  To minimize biological variations, we pooled RNA from two perfused liver samples to use in each array analysis.  The conditions were total and polysome fraction of Perk+/+, -tBuHQ or +tBuHQ; total and polysome fraction of Perk-/-, -tBuHQ or +tBuHQ.  Each array analysis was done in duplicate."
GSE11684_series_matrix.txtimp_info.txt
GCN2 r is 2 
Found activation in !Series_summary	"We use array analysis to determine the global mRNA shift into polysomes following a stress response, and to compare the translational response following activation of GCN2 versus PERK, two of the four eIF2alpha kinases."
GSE11685_series_matrix.txtimp_info.txt
GCN2 r is 2 
Found activation in !Series_title	"Translational response following activation of GCN2 versus PERK"
GSE11685_series_matrix.txtimp_info.txt
GCN2 r is 2 
Found activation in !Series_summary	"We use array analysis to determine the global mRNA shift into polysomes following a stress response, and to compare the translational response following activation of GCN2 versus PERK, two of the four eIF2alpha kinases."
GSE11698_series_matrix.txtimp_info.txt
Trex1 r is 4 
Found KO in !Series_title	"Microarray of Trex1 WT and Trex1 KO hearts on RAG2KO background"
GSE11702_series_matrix.txtimp_info.txt
beta1 r is 5 
Found treated in !Series_overall_design	"Primary osteoblasts cultured under serum-starved condition were treated or untreated with TGF-beta1 for 24 hr."
GSE11702_series_matrix.txtimp_info.txt
TGF-beta1 r is 4 
Found treated in !Series_overall_design	"Primary osteoblasts cultured under serum-starved condition were treated or untreated with TGF-beta1 for 24 hr."
GSE11726_series_matrix.txtimp_info.txt
CN r is 5 
Found loss of in !Series_summary	"We analyzed whether cochlear removal-induced transcriptional changes in the cochlear nucleus (CN) were due to loss of electrical activity in the 8th nerve.  Pharmacological activity blockade of the auditory nerve for 24 h resulted in similar expression changes for only a subset of genes.  Thus, an additional factor not dependent on action potential-mediated signaling must also regulate transcriptional responses to deafferentation in the CN.  "
GSE11726_series_matrix.txtimp_info.txt
CN r is 8 
Found induced in !Series_summary	"We analyzed whether cochlear removal-induced transcriptional changes in the cochlear nucleus (CN) were due to loss of electrical activity in the 8th nerve.  Pharmacological activity blockade of the auditory nerve for 24 h resulted in similar expression changes for only a subset of genes.  Thus, an additional factor not dependent on action potential-mediated signaling must also regulate transcriptional responses to deafferentation in the CN.  "
GSE11756_series_matrix.txtimp_info.txt
Twist r is 1 
Found + in !Series_title	"Comparison of primary MEF vs HRasV12 + Twist transformed MEF"
GSE11766_series_matrix.txtimp_info.txt
Myb r is 5 
Found activation in !Series_summary	"Levels of C/EBPα are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis.  To assess the mechanisms involved in these effects, C/EBPα targets were identified  by microarray analyses.  Upon C/EBPα activation, expression of c-Myb and GATA-2 was  repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly   in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBPα was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBPα while c-Myb siRNA treatment enhanced C/EBPα-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic  differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPα but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPα induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPα activation. In summary, the effects of C/EBPα in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2.  Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPα appear to involve different transcription-regulated targets."
GSE11766_series_matrix.txtimp_info.txt
p210 r is 2 
Found expressing in !Series_title	"Transcriptional repression of c-Myb and GATA-2 is involved in the effects of C/EBPα in p210 BCR/ABL-expressing cells"
GSE11770_series_matrix.txtimp_info.txt
DGK r is 2 
Found induced in !Series_overall_design	"single time point analysis of gene expression changes induced by DGK-zeta transfection in C2C12 cells. DGK-zeta-transfected cells are compared to untreated control cells and to EGFP-transfected cells."
GSE11770_series_matrix.txtimp_info.txt
DGK-zeta r is 2 
Found induced in !Series_overall_design	"single time point analysis of gene expression changes induced by DGK-zeta transfection in C2C12 cells. DGK-zeta-transfected cells are compared to untreated control cells and to EGFP-transfected cells."
GSE11775_series_matrix.txtimp_info.txt
Foxp3 r is 1 
Found mutant in !Series_overall_design	"To identify candidate genes that might be related to the suppressive activity, the Treg cells expressing functional and mutant Foxp3 transcription factor were compared"
GSE11775_series_matrix.txtimp_info.txt
Foxp3 r is 4 
Found expressing in !Series_overall_design	"To identify candidate genes that might be related to the suppressive activity, the Treg cells expressing functional and mutant Foxp3 transcription factor were compared"
GSE11777_series_matrix.txtimp_info.txt
erythropoietin r is 4 
Found -/- in !Series_summary	"Iron is essential for all cells but is toxic in excess, so iron absorption and distribution are tightly regulated.  Serum iron is bound to transferrin and primarily enters erythroid cells via receptor-mediated endocytosis of the transferrin receptor (Tfr1).  Tfr1 is essential for developing erythrocytes and reduced Tfr1 expression is associated with anemia.  The transcription factors STAT5A/B are activated by many cytokines, including erythropoietin.  Stat5a/b-/- mice are severely anemic and die perinatally, but no link has been made to iron homeostasis.  To study the function of STAT5A/B in vivo, we deleted the floxed Stat5a/b locus in hematopoietic cells with a Tie2-Cre transgene.  These mice exhibited microcytic, hypochromic anemia, as did lethally irradiated mice transplanted with Stat5a/b-/- fetal liver cells.  Flow cytometry and RNA analyses of erythroid cells from mutant mice revealed a 50% reduction in Tfr1 mRNA and protein.  We detected STAT5A/B binding sites in the first intron of the Tfr1 gene and found that expression of constitutively active STAT5A in an erythroid cell line increased Tfr1 levels.  Chromatin immunoprecipitation experiments confirmed the binding of STAT5A/B to these sites.  We conclude that STAT5A/B is an important regulator of erythroid progenitor iron uptake via its control of Tfr1 transcription."
GSE11788_series_matrix.txtimp_info.txt
norepinephrine transporter r is 2 
Found deficient in !Series_summary	"Results: We have determined by long serial analysis of gene expression (LongSAGE) the gene expression profiles of in vitro differentiating wild type and norepinephrine transporter-deficient (NETKO) neural crest derivatives. Comparison analyses with the wild type library (GSM 105765) have identified a number of important differentially expressed genes, including genes relevant to noradrenergic neuron differentiation and to the phenotype of NETKO mice. Furthermore we have identified novel differentially expressed genes."
GSE11788_series_matrix.txtimp_info.txt
NET r is 3 
Found deletion in !Series_summary	"Background: The goal of this study was to determine the transcriptional consequences of norepinephrine transporter (NET) gene deletion in noradrenergic neuron differentiation. The norepinephrine transporter (NET) is the target of powerful mind-altering substances, such as tricyclic antidepressants and the drug of abuse, cocaine. NET function in adult noradrenergic neurons of the peripheral and central nervous systems is that of a scavenger that internalizes norepinephrine from the synaptic cleft. By contrast, norepinephrine (NE) transport has a different role in embryogenesis. It promotes differentiation of neural crest cells and locus ceruleus progenitors into noradrenergic neurons, whereas NET inhibitors, such as the tricyclic antidepressant desipramine and the drug of abuse, cocaine, inhibit noradrenergic differentiation. While NET structure und regulation of NET function is well described, little is known about downstream targets of NE transport."
GSE11788_series_matrix.txtimp_info.txt
norepinephrine transporter r is 6 
Found deletion in !Series_summary	"Background: The goal of this study was to determine the transcriptional consequences of norepinephrine transporter (NET) gene deletion in noradrenergic neuron differentiation. The norepinephrine transporter (NET) is the target of powerful mind-altering substances, such as tricyclic antidepressants and the drug of abuse, cocaine. NET function in adult noradrenergic neurons of the peripheral and central nervous systems is that of a scavenger that internalizes norepinephrine from the synaptic cleft. By contrast, norepinephrine (NE) transport has a different role in embryogenesis. It promotes differentiation of neural crest cells and locus ceruleus progenitors into noradrenergic neurons, whereas NET inhibitors, such as the tricyclic antidepressant desipramine and the drug of abuse, cocaine, inhibit noradrenergic differentiation. While NET structure und regulation of NET function is well described, little is known about downstream targets of NE transport."
GSE11803_series_matrix.txtimp_info.txt
PPARdelta r is 4 
Found treated in !Series_summary	"We measured global skeletal muscle expression in sedentary and exercised mice treated with vehicle or PPARdelta ligand GW1516.  PPARdelta is a transcriptional regulator of muscle oxidative metabolism and fatigue resistance."
GSE11804_series_matrix.txtimp_info.txt
PPARdelta r is 8 
Found treated in !Series_summary	"We have conducted skeletal muscle microarrays from mice treated with AMPK agoinst (AICAR), PPARdelta agonist (GW1516) or the combination of the two drugs to investigate the individual and interactive effects of the two on muscle genes."
GSE11808_series_matrix.txtimp_info.txt
NT r is 5 
Found treated in !Series_overall_design	"We established four different groups of mice; non-tumor-bearing and treated with vehicle alone (NT-Co), non-tumor-bearing and treated with TSU68 (NT-TSU), tumor-bearing and treated with vehicle (T-Co), and tumor-bearing and treated with TSU68 (T-TSU). NT-Co, T-Co and T-TSU group were applied to microarray analysis."
GSE11809_series_matrix.txtimp_info.txt
Ifng r is 1 
Found -/- in !Series_summary	"The data from the Ifng-/- experiment have been described (Aly et al. 2007. J Pathol 212:295)."
GSE11809_series_matrix.txtimp_info.txt
Ifng r is 1 
Found -/- in !Series_overall_design	"In two independent blocks of experiments, Ifng-/- and Irf1-/- mice on a C57Bl/6 background and their respective controls were infected with Mycobacterium avium via aerosol. After 14 weeks, mice were sacrificed and the lung RNA prepared using TriFast FL (Peqlab). Total RNA (1µg) was labeled and hybridized to Affymetrix mouse MOE430A 2.0 GeneChips according to the manufacturer’s recommendations. For each condition three biological replicates (except Ifng-/-, no infection) were used. Total of 23 Samples."
GSE11809_series_matrix.txtimp_info.txt
Irf1 r is 3 
Found -/- in !Series_overall_design	"In two independent blocks of experiments, Ifng-/- and Irf1-/- mice on a C57Bl/6 background and their respective controls were infected with Mycobacterium avium via aerosol. After 14 weeks, mice were sacrificed and the lung RNA prepared using TriFast FL (Peqlab). Total RNA (1µg) was labeled and hybridized to Affymetrix mouse MOE430A 2.0 GeneChips according to the manufacturer’s recommendations. For each condition three biological replicates (except Ifng-/-, no infection) were used. Total of 23 Samples."
GSE11821_series_matrix.txtimp_info.txt
Igf-1 r is 3 
Found -/- in !Series_title	"Expression data from Igf-1 -/- and Igf-1+/+ mouse cochleas"
GSE11821_series_matrix.txtimp_info.txt
Igf1 r is 1 
Found -/- in !Series_summary	"Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons."
GSE11821_series_matrix.txtimp_info.txt
Igf-1 r is 6 
Found -/- in !Series_summary	"We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes."
GSE11821_series_matrix.txtimp_info.txt
Igf-1 r is 7 
Found -/- in !Series_overall_design	"Cochleae from two E18.5 were isolated from both Igf-1+/+ wild type and Igf-1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos 18.5 days post coitus (E18.5). Three independent pools were used. Cochlear tissues included the otic capsule but not vestibular tissues."
GSE11836_series_matrix.txtimp_info.txt
Pten r is 1 
Found mutant in !Series_summary	"In our investigations of the molecular pathways of prostate tumorigenesis in Nkx3.1; Pten mutant mice using gene expression profiling, we now find that the AP-1 transcription factors, c-Jun and c-Fos, are significantly up-regulated during cancer progression. Forced expression of c-Fos and c-Jun in prostate cancer cells results in increased tumorigenicity, activation of Erk MAP kinase, and enhanced survival in the absence of androgens, which are hallmarks of disease progression. In humans, Jun and Fos proteins are significantly up-regulated during prostate cancer progression and significantly correlated with activation of Erk MAP kinase. Most notably, expression of Jun is associated with disease recurrence independent of other currently used prognostic indicators."
GSE11836_series_matrix.txtimp_info.txt
Pten r is 2 
Found mutant in !Series_overall_design	"Mouse prostate was collected from wild-type or the Nkx3.1; Pten compound mutant mice at the age of 8-16 months. One lobe of dosolateral prostate was snap-frozen in OCT and stored at -80ºC for laser capture microdissection (LCM). To obtain androgen-independent lesions, mice were castrated at 7 to 14 months of age. Mice were sacrificed for analysis at 8 to 16 months of age and one dosolateral prostatic lobe was snap-frozen in OCT and stored at -80ºC for LCM. Approximate 1000 Prostate epithelial cells were isolated from normal prostate, dysplasia, prostatic intraepithelial neoplasia (PIN) or cancer lesions using PixCell IIE LCM system (Arcturus), followed by RNA linear amplification and labeling using Small Sample Labeling Protocol VII (Affymetrix). Samples were labeled using a BioArray High Yield RNA transcript labeling kit (Enzo Life Scientific) and were hybridized to MOE430A GeneChips containing 22,690 well characterized mouse genes/ESTs (Affymetrix)."
GSE11836_series_matrix.txtimp_info.txt
Erk r is 2 
Found activation in !Series_summary	"In our investigations of the molecular pathways of prostate tumorigenesis in Nkx3.1; Pten mutant mice using gene expression profiling, we now find that the AP-1 transcription factors, c-Jun and c-Fos, are significantly up-regulated during cancer progression. Forced expression of c-Fos and c-Jun in prostate cancer cells results in increased tumorigenicity, activation of Erk MAP kinase, and enhanced survival in the absence of androgens, which are hallmarks of disease progression. In humans, Jun and Fos proteins are significantly up-regulated during prostate cancer progression and significantly correlated with activation of Erk MAP kinase. Most notably, expression of Jun is associated with disease recurrence independent of other currently used prognostic indicators."
GSE11844_series_matrix.txtimp_info.txt
Igf1 r is 1 
Found -/- in !Series_summary	"Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons."
GSE11844_series_matrix.txtimp_info.txt
Igf-1 r is 6 
Found -/- in !Series_summary	"We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes."
GSE11844_series_matrix.txtimp_info.txt
Igf-1 r is 7 
Found -/- in !Series_overall_design	"Cochleae from two E18.5 were isolated from both Igf-1+/+ wild type and Igf-1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos 18.5 days post coitus (E18.5). Three independent pools were used. Cochlear tissues included the otic capsule but not vestibular tissues."
GSE11844_series_matrix.txtimp_info.txt
Igf1 r is 1 
Found null in !Series_title	"Mouse Igf1 null publication analysis"
GSE11859_series_matrix.txtimp_info.txt
Gfap r is 5 
Found expressing in !Series_summary	"Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors."
GSE11859_series_matrix.txtimp_info.txt
Olig2 r is 7 
Found expressing in !Series_summary	"Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors."
GSE11867_series_matrix.txtimp_info.txt
Dll1 r is 1 
Found mutant in !Series_title	"Expression Profiling of Dll1 mutant mouse lines on different genetic background"
GSE11867_series_matrix.txtimp_info.txt
Dll1 r is 1 
Found mutant in !Series_summary	"The two analysed Dll1 mutant mouse lines carry the same mutation but are on different genetic background: 1. Heterozygous F1-animals were backcrossed several times to the 129SV/J wild type; 2. Heterozygous F1-animals were outcrossed 11 generation to C3HeB/FeJ wild type"
GSE11867_series_matrix.txtimp_info.txt
Dll1 r is 1 
Found mutant in !Series_overall_design	"Four organs (liver, spleen, thymus, brain) of two Dll1 mutant mouse lines on different genetic background carrying the same mutation were analysed by cDNA microarray technology. Experiment include 4-5 biological replicates for reference (wildtype) and mutant animals. Up to 4 technical replicates for each mutant mouse were performed. As reference pooled RNA was used. 50% of the chip hybridisations are dye sway experiments."
GSE11884_series_matrix.txtimp_info.txt
Furin r is 1 
Found deficient in !Series_summary	"Furin is a proprotein convertase induced in activated T cells, reported to processes the anti-inflammatory cytokine TGFb-1.  Herein, we show that conditional deletion of furin in T cells allowed for normal T cell development but impaired the function of regulatory T cells and effector cells, which produced less TGFb-1.  Furin-deficient Treg cells, were less protective in a T cell transfer colitis model and failed to induce Foxp3 in normal T cells. Furin-deficient effector cells were inherently overly active and were resistant to suppressive activity of wild-type Tregs. Thus, our results indicate that furin is indispensable in maintaining peripheral tolerance, which is due, at least in part, to its nonredundant, essential function in regulating TGFb-1 production.  Targeting furin has emerged as a strategy in malignant and infectious disease.  The current work suggests that inhibiting furin might activate immune responses, but may result in a breakdown in peripheral tolerance. "
GSE11884_series_matrix.txtimp_info.txt
furin r is 2 
Found deletion in !Series_summary	"Furin is a proprotein convertase induced in activated T cells, reported to processes the anti-inflammatory cytokine TGFb-1.  Herein, we show that conditional deletion of furin in T cells allowed for normal T cell development but impaired the function of regulatory T cells and effector cells, which produced less TGFb-1.  Furin-deficient Treg cells, were less protective in a T cell transfer colitis model and failed to induce Foxp3 in normal T cells. Furin-deficient effector cells were inherently overly active and were resistant to suppressive activity of wild-type Tregs. Thus, our results indicate that furin is indispensable in maintaining peripheral tolerance, which is due, at least in part, to its nonredundant, essential function in regulating TGFb-1 production.  Targeting furin has emerged as a strategy in malignant and infectious disease.  The current work suggests that inhibiting furin might activate immune responses, but may result in a breakdown in peripheral tolerance. "
GSE11897-GPL1261_series_matrix.txtimp_info.txt
Nobox r is 4 
Found loss of in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL1261_series_matrix.txtimp_info.txt
Pou5f1 r is 7 
Found loss of in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL1261_series_matrix.txtimp_info.txt
Lhx8 r is 1 
Found knockout in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL339_series_matrix.txtimp_info.txt
Nobox r is 4 
Found loss of in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL339_series_matrix.txtimp_info.txt
Pou5f1 r is 7 
Found loss of in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL339_series_matrix.txtimp_info.txt
Lhx8 r is 1 
Found knockout in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL340_series_matrix.txtimp_info.txt
Nobox r is 4 
Found loss of in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL340_series_matrix.txtimp_info.txt
Pou5f1 r is 7 
Found loss of in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11897-GPL340_series_matrix.txtimp_info.txt
Lhx8 r is 1 
Found knockout in !Series_summary	"Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway."
GSE11899_series_matrix.txtimp_info.txt
Afp r is 5 
Found deletion in !Series_summary	"Background & Aims: MiRNAs are small (~22 nucleotide), non-coding RNA molecules that regulate gene expression through imperfect complementarity with target messenger RNAs. The function of miRNA in mammalian organogenesis is largely unknown. Conditional loss-of-function of Dicer, the enzyme that processes precursor miRNA transcripts into their mature, active form, has been shown to cause severe defects in a number of organ systems. Here we address the role of Dicer in liver development and function. Methods: Mice lacking Dicer function in hepatocytes were generated using an Afp-Cre strain to drive deletion of a floxed Dicer allele. Deletion of the flox-dicer allele was confirmed by quantitative PCR. Decreased miRNA levels detected by quantitative RT-PCR and in situ hybridization confirmed loss of Dicer function. Gene expression microarray analysis was performed on liver RNA from P28 mutant and control mice. Liver sections from mutant and control mice ranging from embryonic stages through 3-4 months of age were examined and liver function tests were performed on adult mice. Results: Mice lacking hepatocyte Dicer function were born alive at the expected frequency, and had grossly normal appearance and behavior. Despite the loss of mature miRNA, hepatic function was normal, as reflected by normal blood gludose, albumin, cholesterol, and bilirubin. However, mutant mice between 2-4 months of age exhibit progressive hepatocyte damage, elevated ALT/AST, with evidence of balanced proliferation and apoptosis in the lobule. Microarray analysis indicates large-scale changes in gene expression, with increased expression of many miRNA targets, as well as imprinted genes. Conclusions: Loss of miRNA processing in the liver at late gestation has a remarkably mild phenotype, suggesting that miRNAs do not play an essential role in hepatic physiology. However, miRNA deficiency results in hepatocyte apoptosis and balanced hepatocyte regeneration. Finally, microarray analysis of gene expression in mutant liver suggests a previously unrecognized role for Dicer in the repression of imprinted genes."
GSE11911_series_matrix.txtimp_info.txt
ovalbumin r is 1 
Found induced in !Series_summary	"Methods: In an ovalbumin-induced murine model of asthma we applied microarray gene expression analysis of the lung at different time points in the asthmatic process. Advanced statistical methods were used to relate gene expression changes to cellular processes and to integrate our results into multiple levels of information available in public databases. "
GSE11924_series_matrix.txtimp_info.txt
Th r is 6 
Found activation in !Series_summary	"After activation, CD4+ helper T (Th) cells differentiate"
GSE11924_series_matrix.txtimp_info.txt
Th r is 6 
Found activation in !Series_summary	"After activation, CD4+ helper T (Th) cells differentiate"
GSE11935_series_matrix.txtimp_info.txt
LIF r is 1 
Found -/- in !Series_summary	"Oligodendrocyte precursor cells from postnatal day 10 optic nerve remained in a developmentally immature state in LIF-/- mice.  Partial recovery of myelin genes is seen in LIF-/- mice by postnatal day 14 in the optic nerve.  Very little difference in myelin genes in the optic nerve is seen by postnatal day 35 (adult)."
GSE11963_series_matrix.txtimp_info.txt
p50 r is 3 
Found activation in !Series_summary	"Background: Lymphotoxin signaling via the lymphotoxin-β receptor (LTβR) has been implicated in several biological processes, ranging from development of secondary lymphoid organs, maintenance of splenic tissue, host defense against pathogens, autoimmunity, and lipid homeostasis. The major transcription factor that is activated by LTβR crosslinking is NF-κB. Two signaling pathways have been described that result in the activation of classical p50-RelA and alternative p52-RelB NF-κB heterodimers."
GSE11963_series_matrix.txtimp_info.txt
p52 r is 7 
Found activation in !Series_summary	"Background: Lymphotoxin signaling via the lymphotoxin-β receptor (LTβR) has been implicated in several biological processes, ranging from development of secondary lymphoid organs, maintenance of splenic tissue, host defense against pathogens, autoimmunity, and lipid homeostasis. The major transcription factor that is activated by LTβR crosslinking is NF-κB. Two signaling pathways have been described that result in the activation of classical p50-RelA and alternative p52-RelB NF-κB heterodimers."
GSE11973_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_title	"Wild-type cultured neutrophils versus miR-223 null cultured neutrophils "
GSE11973_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_summary	"This array analysis is to study the regulation of target messages’ expression in in vitro cultured murine neutrophils versus miR-223 null neutrophils.  Culture media was SILAC-IMDM for MS analysis."
GSE11973_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_overall_design	"Wild-type cultured neutrophils versus miR-223 null cultured neutrophils "
GSE11982_series_matrix.txtimp_info.txt
E2A r is 1 
Found KO in !Series_title	"Expression data from WT and E2A-KO bone marrow stem and progenitor cell subfractions."
GSE11982_series_matrix.txtimp_info.txt
E2A r is 1 
Found KO in !Series_summary	"Expression profiling of WT and E2A-KO LSK FLT3- and LMPP protenitor cells."
GSE11982_series_matrix.txtimp_info.txt
E2A r is 1 
Found KO in !Series_overall_design	"LSK FLT3- and LMPP stem/progenitor cells from WT and E2A-KO mice were FACS sorted. Subsequently RNA was extracted, labelled and hybridized to Affymetrix microarrays. Goal of experiment was to investigate expression changes between WT and KO LMPP cells."
GSE11990_series_matrix.txtimp_info.txt
p53 r is 1 
Found deficient in !Series_title	"Gene expression profiling of mouse p53-deficient epidermal carcinoma defines molecular determinants of human cancer malignancy (training dataset)"
GSE12001_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_title	"Wild-type neutrophils and miR-223 null neutrophils"
GSE12001_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_summary	"This array analysis is to study the regulation of target messages’ expression in murine neutrophils versus miR-223 null neutrophils.  "
GSE12001_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_overall_design	"Three arrays for wild-type neutrophils and miR-223 null neutrophils"
GSE12003_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_title	"4 days cultured progenitors and 8 days cultured mature neutrophils from WT vs miR-223 null neutrophils"
GSE12003_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_summary	"This array analysis is to study developmental time course of the regulation of target messages’ expression during culture of murine neutrophils versus miR-223 null neutrophils.  Culture media was SILAC-IMDM for MS analysis."
GSE12003_series_matrix.txtimp_info.txt
miR-223 r is 2 
Found null in !Series_overall_design	"Two arrays of each for 4 days cultured progenitors and 8 days cultured mature neutrophils from wild-type cultured neutrophils versus miR-223 null cultured neutrophils"
GSE12008-GPL4134_series_matrix.txtimp_info.txt
p65 r is 3 
Found knock-out in !Series_summary	"LMX1B is a LIM-homeodomain transcription factor essential for development. Putative LMX1B target genes have been identified through mouse gene targeting studies; however, in the absence of in vivo molecular characterization of their regulation, their identity as direct LMX1B targets remains hypothetical. We describe here the first molecular characterization of LMX1B target gene regulation. A tetracycline-inducible expression system and microarray analysis showed that a subset of NF-kappa B target genes, including IL-6 and IL-8 are upregulated in LMX1B-expressing HeLa cells. Chromatin immunoprecipitation assays revealed that LMX1B binds to the proximal promoter region of IL-6 and IL-8 in vivo, in the vicinity of the characterized kappa B site, and that LMX1B recruitment correlates with an increased NF-kappa B DNA association. Inhibition of NF-kappa B activity by short interfering RNA-mediated knock-down of p65 impairs LMX1B-dependent induction of NF-kappa B target genes, while activation of NF-kappa B activity by TNF-alpha results in a synergistic induction of these genes by LMX1B. IL-6 promoter-driven reporter assays showed that the kappa B site and an adjacent putative LMX1B binding motif are both involved in LMX1B-mediated transcription. Expression of a number of NF-kappa B target genes is affected in the kidney of Lmx1b-/- knock-out mice, thus supporting the biological relevance of the data obtained in the human cell line. Together, these data demonstrate for the first time that LMX1B directly regulates transcription of a subset of NF-kappa B target genes in cooperation with nuclear p50/p65 NF-kappa B."
GSE12008-GPL4134_series_matrix.txtimp_info.txt
Lmx1b r is 3 
Found knock-out in !Series_overall_design	"Mouse subset (GSM304379-GSM304384): Three kidney samples from newborn wild-type mice and from newborn Lmx1b-/- knock-out mice were processed for gene expression array analyses using an Agilent platform."
GSE12008-GPL4134_series_matrix.txtimp_info.txt
Lmx1b r is 1 
Found -/- in !Series_summary	"LMX1B is a LIM-homeodomain transcription factor essential for development. Putative LMX1B target genes have been identified through mouse gene targeting studies; however, in the absence of in vivo molecular characterization of their regulation, their identity as direct LMX1B targets remains hypothetical. We describe here the first molecular characterization of LMX1B target gene regulation. A tetracycline-inducible expression system and microarray analysis showed that a subset of NF-kappa B target genes, including IL-6 and IL-8 are upregulated in LMX1B-expressing HeLa cells. Chromatin immunoprecipitation assays revealed that LMX1B binds to the proximal promoter region of IL-6 and IL-8 in vivo, in the vicinity of the characterized kappa B site, and that LMX1B recruitment correlates with an increased NF-kappa B DNA association. Inhibition of NF-kappa B activity by short interfering RNA-mediated knock-down of p65 impairs LMX1B-dependent induction of NF-kappa B target genes, while activation of NF-kappa B activity by TNF-alpha results in a synergistic induction of these genes by LMX1B. IL-6 promoter-driven reporter assays showed that the kappa B site and an adjacent putative LMX1B binding motif are both involved in LMX1B-mediated transcription. Expression of a number of NF-kappa B target genes is affected in the kidney of Lmx1b-/- knock-out mice, thus supporting the biological relevance of the data obtained in the human cell line. Together, these data demonstrate for the first time that LMX1B directly regulates transcription of a subset of NF-kappa B target genes in cooperation with nuclear p50/p65 NF-kappa B."
GSE12008-GPL4134_series_matrix.txtimp_info.txt
Lmx1b r is 1 
Found -/- in !Series_overall_design	"Mouse subset (GSM304379-GSM304384): Three kidney samples from newborn wild-type mice and from newborn Lmx1b-/- knock-out mice were processed for gene expression array analyses using an Agilent platform."
GSE12008-GPL4134_series_matrix.txtimp_info.txt
TNF-alpha r is 7 
Found activation in !Series_summary	"LMX1B is a LIM-homeodomain transcription factor essential for development. Putative LMX1B target genes have been identified through mouse gene targeting studies; however, in the absence of in vivo molecular characterization of their regulation, their identity as direct LMX1B targets remains hypothetical. We describe here the first molecular characterization of LMX1B target gene regulation. A tetracycline-inducible expression system and microarray analysis showed that a subset of NF-kappa B target genes, including IL-6 and IL-8 are upregulated in LMX1B-expressing HeLa cells. Chromatin immunoprecipitation assays revealed that LMX1B binds to the proximal promoter region of IL-6 and IL-8 in vivo, in the vicinity of the characterized kappa B site, and that LMX1B recruitment correlates with an increased NF-kappa B DNA association. Inhibition of NF-kappa B activity by short interfering RNA-mediated knock-down of p65 impairs LMX1B-dependent induction of NF-kappa B target genes, while activation of NF-kappa B activity by TNF-alpha results in a synergistic induction of these genes by LMX1B. IL-6 promoter-driven reporter assays showed that the kappa B site and an adjacent putative LMX1B binding motif are both involved in LMX1B-mediated transcription. Expression of a number of NF-kappa B target genes is affected in the kidney of Lmx1b-/- knock-out mice, thus supporting the biological relevance of the data obtained in the human cell line. Together, these data demonstrate for the first time that LMX1B directly regulates transcription of a subset of NF-kappa B target genes in cooperation with nuclear p50/p65 NF-kappa B."
GSE12025_series_matrix.txtimp_info.txt
M3 r is 5 
Found induced in !Series_summary	"Endocrine enriched genes in adult islet beta cells were identified and compared with that of induced beta cells (with M3 transcription factors) in adult.  The control sample is non-beta pancreatic cells."
GSE12028_series_matrix.txtimp_info.txt
interleukin-10 r is 3 
Found deficient in !Series_title	"Modulation of colon inflammation in interleukin-10 gene-deficient mice via dietary polyunsaturated fatty acid"
GSE12028_series_matrix.txtimp_info.txt
Il10 r is 2 
Found deficient in !Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."
GSE12028_series_matrix.txtimp_info.txt
interleukin-10 r is 3 
Found deficient in !Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."
GSE12028_series_matrix.txtimp_info.txt
Il10 r is 1 
Found -/- in !Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."
GSE12028_series_matrix.txtimp_info.txt
interleukin-10 r is 6 
Found -/- in !Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."
GSE12028_series_matrix.txtimp_info.txt
Ppara r is 3 
Found activation in !Series_summary	"Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins."
GSE12067_series_matrix.txtimp_info.txt
immediate early r is 7 
Found exposure in !Series_summary	"The growth factor interleukin-3 (IL-3) promotes the survival and growth of multipotent hematopoietic progenitors and stimulates myelopoiesis.  It has also been reported to oppose terminal granulopoiesis and to support leukemic cell growth through autocrine or paracrine mechanisms.  We used kinetic microarray, Northern Blotting and bioinformatics analysis of IL-3 dependent myeloblasts to determine whether IL-3 acts in part by regulating the rate of turnover of mRNA transcripts in specific functional pathways.  Our results indicate that exposure of myeloblasts to IL-3 causes immediate early stabilization of hundreds of transcripts in pathways relevant to myeloblast function.  Examples include transcripts associated with proliferation and leukemic transformation (pik3cd, myb, pim-1), hematopoietic development (cited2), differentiation control (cdkn1a) and RNA processing (BRF1, BRF2).  A domain in the 3’-utr of IL-6 that mediates IL-3 responsiveness contains AU-rich elements that bind proteins known to modulate mRNA stability, however a known destabilizing protein (AUF1) is shown not to mediate degradation in the absence of IL-3.    These findings support a model of IL-3 action through mRNA stability control and suggest that aberrant stabilization of this network of transcripts could contribute to growth patterns observed in leukemia."
GSE12073_series_matrix.txtimp_info.txt
Aire r is 1 
Found expressing in !Series_title	"Expression data from transgenic Aire expressing pancreatic islets"
GSE12134_series_matrix.txtimp_info.txt
Tbr2 r is 8 
Found loss of in !Series_summary	"mid-neurogenesis and gain-of-function experiments show that AP2γ directly regulates the expression of several genes characteristic for basal progenitors, such as Math3 and Tbr2. The misspecification of basal progenitors upon loss of AP2γ resulted in their increased death and"
GSE12135_series_matrix.txtimp_info.txt
Emx2 r is 3 
Found knockout in !Series_title	"Expression data from Emx2 wildtype and knockout olfactory epithelium"
GSE12135_series_matrix.txtimp_info.txt
Emx2 r is 1 
Found knockout in !Series_summary	"Emx2 is a homeobox transcription factor that plays a critical role in development. Olfactory sensory neuron axons from Emx2 knockout mice fail to innervate their target tissue, the olfactory bulb. Homeobox transcription factors may also play an important role in olfactory receptor expression."
GSE12135_series_matrix.txtimp_info.txt
Emx2 r is 3 
Found knockout in !Series_summary	"We used microarrays to analyze differences in mRNA abundance in the olfactory epithelium of Emx2 wildtype and knockout embryonic day 18.5 mice."
GSE12135_series_matrix.txtimp_info.txt
Emx2 r is 5 
Found knockout in !Series_overall_design	"Total RNA from 9 Emx2 wildtype and 9 Emx2 knockout mice was analyzed. Equal amounts of RNA from 3 animals was pooled to create one biological sample, 3 pools per genotype, 6 chips total. RNA was hybridized to the Affymetrix Mouse Exon 1.0 ST array."
GSE12147_series_matrix.txtimp_info.txt
triglycerides r is 8 
Found induced in !Series_summary	"The nuclear receptor PPARalpha is recognized as the primary target of the fibrate class of hypolipidemic drugs and mediates lipid lowering in part by activating a transcriptional cascade that induces genes involved in the catabolism of lipids.  We report here the characterization of three novel PPARalpha agonists with therapeutic potential for treating dyslipidemia.  These structurally related compounds display potent and selective binding to human PPARalpha and support robust recruitment of coactivator peptides in vitro.  These compounds markedly potentiate chimeric transcription systems in cell-based assays and strikingly lower serum triglycerides in vivo.  The transcription networks induced by these selective PPARalpha agonists were assessed by transcriptional profiling of mouse liver after acute and chronic treatment.  The induction of several known PPARalpha target genes involved with fatty acid metabolism were observed, reflecting the expected pharmacology associated with PPARalpha activation.  We also noted the downregulation of a number of genes related to immune cell function, the acute phase response, and glucose metabolism; suggesting that these compounds may have anti-inflammatory action in the mammalian liver. Taken together, these studies articulate the therapeutic promise of a selective PPARalpha agonist."
GSE12183_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found knockout in !Series_summary	"We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice."
GSE12183_series_matrix.txtimp_info.txt
Mdr2 r is 4 
Found KO in !Series_summary	"We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice."
GSE12185-GPL6096_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found knockout in !Series_summary	"We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice."
GSE12185-GPL6096_series_matrix.txtimp_info.txt
Mdr2 r is 4 
Found KO in !Series_summary	"We crossed the HCV-Tg mice which do not produce HCC with the Mdr2-knockout (Mdr2-KO) mice which develop inflammation-associated HCC, to generate Mdr2-KO/HCV-Tg mice. We studied the effect of the HCV transgene on tumor incidence, hepatocyte mitosis and apoptosis, and on gene expression in the liver of produced mice."
GSE12209_series_matrix.txtimp_info.txt
Crtc1 r is 1 
Found knockout in !Series_overall_design	"Mice were fasted overnight for 18h and refed for 6h.  Hypothalami were obtained from 3 wild-type and 3 Crtc1 knockout mice.  Total RNA was isolated from each sample and equal amounts from each sample were pooled for the microarray."
GSE12209_series_matrix.txtimp_info.txt
Cartpt r is 4 
Found stimulated in !Series_summary	"The adipocyte-derived hormone leptin maintains energy balance by acting on hypothalamic leptin receptors (Leprs) that trigger the signal transducer and activator of transcription 3 (Stat3). Although disruption of Lepr-Stat3 signaling promotes obesity in mice, other features of Lepr function, such as fertility, seem normal, pointing to the involvement of additional regulators. Here we show that the cyclic AMP responsive element–binding protein-1 (Creb1)-regulated transcription coactivator-1 (Crtc1) is required for energy balance and reproduction—Crtc1-/- mice are hyperphagic, obese and infertile. Hypothalamic Crtc1 was phosphorylated and inactive in leptin-deficient ob/ob mice; leptin administration increased amounts of dephosphorylated nuclear Crtc1. Dephosphorylated Crtc1 stimulated expression of the Cartpt and Kiss1 genes, which encode hypothalamic neuropeptides that mediate leptin’s effects on satiety and fertility. Crtc1 overexpression in hypothalamic cells increased Cartpt and Kiss1 gene expression, whereas Crtc1 depletion decreased it. Indeed, leptin enhanced Crtc1 activity over the Cartpt and Kiss1 promoters in cells overexpressing Lepr and these effects were disrupted by expression of a dominant-negative Creb1 polypeptide. As leptin administration increased recruitment of hypothalamic Crtc1 to Cartpt and Kiss1 promoters, our results indicate that the Creb1-Crtc1 pathway mediates the central effects of hormones and nutrients on energy balance and fertility."
GSE12209_series_matrix.txtimp_info.txt
Kiss1 r is 6 
Found stimulated in !Series_summary	"The adipocyte-derived hormone leptin maintains energy balance by acting on hypothalamic leptin receptors (Leprs) that trigger the signal transducer and activator of transcription 3 (Stat3). Although disruption of Lepr-Stat3 signaling promotes obesity in mice, other features of Lepr function, such as fertility, seem normal, pointing to the involvement of additional regulators. Here we show that the cyclic AMP responsive element–binding protein-1 (Creb1)-regulated transcription coactivator-1 (Crtc1) is required for energy balance and reproduction—Crtc1-/- mice are hyperphagic, obese and infertile. Hypothalamic Crtc1 was phosphorylated and inactive in leptin-deficient ob/ob mice; leptin administration increased amounts of dephosphorylated nuclear Crtc1. Dephosphorylated Crtc1 stimulated expression of the Cartpt and Kiss1 genes, which encode hypothalamic neuropeptides that mediate leptin’s effects on satiety and fertility. Crtc1 overexpression in hypothalamic cells increased Cartpt and Kiss1 gene expression, whereas Crtc1 depletion decreased it. Indeed, leptin enhanced Crtc1 activity over the Cartpt and Kiss1 promoters in cells overexpressing Lepr and these effects were disrupted by expression of a dominant-negative Creb1 polypeptide. As leptin administration increased recruitment of hypothalamic Crtc1 to Cartpt and Kiss1 promoters, our results indicate that the Creb1-Crtc1 pathway mediates the central effects of hormones and nutrients on energy balance and fertility."
GSE12223_series_matrix.txtimp_info.txt
sp r is 6 
Found -/- in !Series_title	"Changes in colon gene expression assoc. with increased colon inflam. in IL-10-/- mice inoculated with Enterococcus sp."
GSE12285_series_matrix.txtimp_info.txt
C/EBPbeta r is 8 
Found induced in !Series_summary	"Interleukin-1 (IL-1) is produced from immune-activated cells upon infection and tissue injury, and stimulates a variety of cells expressing its receptor. IL-1 receptor activation results in intracellular signaling cascades that culminate in the activation of transcription factors such as NF-kappaB, AP-1, and C/EBPbeta. To identify genes whose expression is induced in response to IL-1, we performed DNA microarray analysis of IL-1-treated murine dermal fibroblasts (DFs). The gene expression patterns in control, untreated DFs and in DFs treated with IL-1 were compared."
GSE12294_series_matrix.txtimp_info.txt
Tbr2 r is 7 
Found induced in !Series_summary	"Basal (intermediate) progenitors are the major source of neurons in the mammalian cerebral cortex. The molecular machinery governing basal progenitor biogenesis is unknown. Here we show that the zinc finger transcription factor Insm1 (insulinoma-associated 1) is expressed  specifically in progenitors undergoing neurogenic divisions and has a key role in basal progenitor formation. Mouse embryos lacking Insm1 contained half the number of basal progenitors and showed a marked reduction in cortical plate radial thickness. Forced premature expression of Insm1 in neuroepithelial cells resulted in their mitosis occurring at the basal (rather than apical) side of the ventricular zone and induced expression of the basal progenitor marker Tbr2. Remarkably,  these cells remained negative for Tis21, a marker of neurogenic progenitors, and did not generate neurons but underwent self-amplification. Our data imply that Insm1 is involved in the generation  and expansion of basal progenitors, a hallmark of cerebral cortex evolution."
GSE12313_series_matrix.txtimp_info.txt
FU r is 3 
Found treated in !Series_overall_design	"Mll-AF4stop knock-in mice were treated with 5-FU and 5 days later their bone marrow infected ex vivo with either Cre-GFP to activate the Mll-AF4 fusion construct or with a control MIG-Cre retrovirus. GFP+ cells were sorted 2 days post-infection and cultured for 14 days under lymphoid growth conditions before total RNA was isolated for hybridization to Affymetrix expression microarrays."
GSE12315_series_matrix.txtimp_info.txt
Gpx r is 7 
Found loss of in !Series_summary	"Using glutathione peroxidase, Gpx1 and Gpx2, double knockout (Gpx1/2-KO) mice as a model of inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylation and chromatin changing’s in the mouse ileum during chronic inflammation, aging and cancer. We found that inflammation leads to aberrant DNA methylation in Polycomb target genes, with 70% of the ~250 genes methylated in the inflamed tissue being PcG targets in embryonic stem cells and 58% of the methylated genes being marked by H3K27 trimethylation in the ileum of adult wildtype mice. Acquisition of DNA methylation at CpG islands in the ileum of Gpx-1/2-KO mice frequently correlated with loss of H3K27 trimethylation at the same loci. Inflammation-associated DNA methylation occurs preferentially in tissue-specific silent genes and, importantly, is much more frequently represented in tumors than is age-dependent DNA methylation. 60% of aberrant methylation found in tumors is also present in the inflamed tissue. In summary, inflammation creates a signature of aberrant DNA methylation, which is observed later in the malignant tissue and is directed by the PcG complex."
GSE12315_series_matrix.txtimp_info.txt
Gpx1 r is 5 
Found knockout in !Series_summary	"Using glutathione peroxidase, Gpx1 and Gpx2, double knockout (Gpx1/2-KO) mice as a model of inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylation and chromatin changing’s in the mouse ileum during chronic inflammation, aging and cancer. We found that inflammation leads to aberrant DNA methylation in Polycomb target genes, with 70% of the ~250 genes methylated in the inflamed tissue being PcG targets in embryonic stem cells and 58% of the methylated genes being marked by H3K27 trimethylation in the ileum of adult wildtype mice. Acquisition of DNA methylation at CpG islands in the ileum of Gpx-1/2-KO mice frequently correlated with loss of H3K27 trimethylation at the same loci. Inflammation-associated DNA methylation occurs preferentially in tissue-specific silent genes and, importantly, is much more frequently represented in tumors than is age-dependent DNA methylation. 60% of aberrant methylation found in tumors is also present in the inflamed tissue. In summary, inflammation creates a signature of aberrant DNA methylation, which is observed later in the malignant tissue and is directed by the PcG complex."
GSE12315_series_matrix.txtimp_info.txt
Gpx2 r is 3 
Found knockout in !Series_summary	"Using glutathione peroxidase, Gpx1 and Gpx2, double knockout (Gpx1/2-KO) mice as a model of inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylation and chromatin changing’s in the mouse ileum during chronic inflammation, aging and cancer. We found that inflammation leads to aberrant DNA methylation in Polycomb target genes, with 70% of the ~250 genes methylated in the inflamed tissue being PcG targets in embryonic stem cells and 58% of the methylated genes being marked by H3K27 trimethylation in the ileum of adult wildtype mice. Acquisition of DNA methylation at CpG islands in the ileum of Gpx-1/2-KO mice frequently correlated with loss of H3K27 trimethylation at the same loci. Inflammation-associated DNA methylation occurs preferentially in tissue-specific silent genes and, importantly, is much more frequently represented in tumors than is age-dependent DNA methylation. 60% of aberrant methylation found in tumors is also present in the inflamed tissue. In summary, inflammation creates a signature of aberrant DNA methylation, which is observed later in the malignant tissue and is directed by the PcG complex."
GSE12315_series_matrix.txtimp_info.txt
Gpx1 r is 8 
Found KO in !Series_summary	"Using glutathione peroxidase, Gpx1 and Gpx2, double knockout (Gpx1/2-KO) mice as a model of inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylation and chromatin changing’s in the mouse ileum during chronic inflammation, aging and cancer. We found that inflammation leads to aberrant DNA methylation in Polycomb target genes, with 70% of the ~250 genes methylated in the inflamed tissue being PcG targets in embryonic stem cells and 58% of the methylated genes being marked by H3K27 trimethylation in the ileum of adult wildtype mice. Acquisition of DNA methylation at CpG islands in the ileum of Gpx-1/2-KO mice frequently correlated with loss of H3K27 trimethylation at the same loci. Inflammation-associated DNA methylation occurs preferentially in tissue-specific silent genes and, importantly, is much more frequently represented in tumors than is age-dependent DNA methylation. 60% of aberrant methylation found in tumors is also present in the inflamed tissue. In summary, inflammation creates a signature of aberrant DNA methylation, which is observed later in the malignant tissue and is directed by the PcG complex."
GSE12315_series_matrix.txtimp_info.txt
Gpx2 r is 6 
Found KO in !Series_summary	"Using glutathione peroxidase, Gpx1 and Gpx2, double knockout (Gpx1/2-KO) mice as a model of inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylation and chromatin changing’s in the mouse ileum during chronic inflammation, aging and cancer. We found that inflammation leads to aberrant DNA methylation in Polycomb target genes, with 70% of the ~250 genes methylated in the inflamed tissue being PcG targets in embryonic stem cells and 58% of the methylated genes being marked by H3K27 trimethylation in the ileum of adult wildtype mice. Acquisition of DNA methylation at CpG islands in the ileum of Gpx-1/2-KO mice frequently correlated with loss of H3K27 trimethylation at the same loci. Inflammation-associated DNA methylation occurs preferentially in tissue-specific silent genes and, importantly, is much more frequently represented in tumors than is age-dependent DNA methylation. 60% of aberrant methylation found in tumors is also present in the inflamed tissue. In summary, inflammation creates a signature of aberrant DNA methylation, which is observed later in the malignant tissue and is directed by the PcG complex."
GSE12337_series_matrix.txtimp_info.txt
PPARalpha r is 1 
Found -/- in !Series_overall_design	"Wild-type and PPARalpha-/- mice were sham-operated or subjected to TAC for 28 days. Left ventricular gene expression profile was determined using Affymetrix 430 2.0 arrays containing over 45,000 probe sets (covering over 34,000 mouse genes) to detect PPARalpha-related differences in cardiac gene expression under basal conditions and after imposition of a sustained hemodynamic stress."
GSE12346_series_matrix.txtimp_info.txt
TCR r is 1 
Found induced in !Series_summary	"Th2 cells enable humoral immunity and host-defense to parasites. Whereas IL-4 drives Th2 differentiation and IL-2 is important later in this process by augmenting IL4 chromatin accessibility, we demonstrate that IL-2 serves an essential early role in regulating IL-4Rα expression by inducing binding of Stat5a and Stat5b to the IL4ra locus, with sustained binding during Th2 differentiation.  Although IL-4 induces IL-4Rα expression, TCR-induced IL-4Rα expression was unexpectedly normal in ILr-/- but profoundly diminished in IL2-/- T cells. Remarkably, enforced IL-4Rα expression rescued Th2 differentiation in IL2-/- cells. These results reveal a novel function for IL-2, with IL-2 via Stat5 providing an early signal for IL4ra induction, thereby priming cells for Th2 differentiation and promoting/maintaining IL-4Rα expression in Th2-committed cells."
GSE12389_series_matrix.txtimp_info.txt
scid r is 2 
Found induced in !Series_summary	"We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. BDC T cells were a mixture of cells expressing high, intermediate and low levels of the T cell receptor. Clonotype-low BDC T cells were required for LTP. Furthermore, islet infiltrating leukocytes in the LTP mice contained Foxp3+CD4 T cells. Islet inflammation in both diabetic and LTP mice was characterized by heavy infiltration of macrophages. Gene expression profiles indicated that macrophages in diabetic mice were M1-type, while LTP mice contained M2-differentiated. The LTP was abolished if mice were treated with either an antibody depleting CD4 T cells, or a neutralizing antibody to CTLA-4, in this case, only at a late stage. Neutralization of IL-10, TGF-β, GITR or CD25 had no effect. Transfer of only clonotype-high expressing BDC T cells induced diabetes but in contrast, H22 antibodies did not inhibit diabetes. While clonotype high T cells induced diabetes even when IFN-γ was neutralized, paradoxically, there was reduced inflammation and no diabetes if host myeloid cells lacked IFN-γ receptor. Hence, using monoclonal CD4 T cells, IFN-γ can have a wide diversity of roles, depending on the setting of the immune process."
GSE12412_series_matrix.txtimp_info.txt
E15 r is 7 
Found knockout in !Series_summary	"The gene expression profiles of control vs AGTR2 knockout mouse whole brains at developmental stage E15 and postnatal day 1 were examined."
GSE12415_series_matrix.txtimp_info.txt
Hsf4 r is 3 
Found lacking in !Series_summary	"Microarray Analyses of Newborn Mouse lens lacking HSF4. Hsf4 is essential for lens development."
GSE12419-GPL2884_series_matrix.txtimp_info.txt
MM r is 4 
Found induced in !Series_summary	"The human CDKN2A locus encodes two distinct proteins, p16(INK4A) and p14(ARF) [mouse p19(Arf)], designated INK4A and ARF herein, that are translated from alternatively spliced mRNAs.  Human ARF is implicated as a tumor suppressor gene, mainly in association with the simultaneous deletion of INK4A.  However, questions remain as to whether loss of ARF alone is sufficient to drive tumorigenesis.  Here we report that mice deficient for Arf are susceptible to accelerated asbestos-induced malignant mesothelioma (MM).  MMs arising in Arf (+/-) mice consistently exhibit biallelic inactivation of Arf, but unexpectedly, do not acquire additional recurrent genetic alterations that we previously identified in asbestos-induced MMs arising in Nf2 (+/-) mice.  Array CGH analysis was used to detect a recurrent deletion at chromosome 4C6.  A candidate in this region, Faf1 (FAS-associated factor 1), was further explored because it encodes a protein implicated in tumor cell survival and in the pathogenesis of some human tumor types.  We confirmed hemizygous loss of Faf1 and down regulation of Faf1 protein in a series of MMs from Arf (+/-) mice, and then showed that Faf1 regulates TNFalpha-mediated NFkappaB signaling, a mechanism previously implicated in asbestos-induced oncogenesis of human mesothelial cells.  Collectively, these investigations divulge important information regarding the significance of Arf inactivation in MM pathogenesis, and implicate Faf1 as a key component in the TNFalpha/NFkappaB signaling node that has now been independently implicated in the asbestos-induced oncogenesis."
GSE12419-GPL4092_series_matrix.txtimp_info.txt
MM r is 4 
Found induced in !Series_summary	"The human CDKN2A locus encodes two distinct proteins, p16(INK4A) and p14(ARF) [mouse p19(Arf)], designated INK4A and ARF herein, that are translated from alternatively spliced mRNAs.  Human ARF is implicated as a tumor suppressor gene, mainly in association with the simultaneous deletion of INK4A.  However, questions remain as to whether loss of ARF alone is sufficient to drive tumorigenesis.  Here we report that mice deficient for Arf are susceptible to accelerated asbestos-induced malignant mesothelioma (MM).  MMs arising in Arf (+/-) mice consistently exhibit biallelic inactivation of Arf, but unexpectedly, do not acquire additional recurrent genetic alterations that we previously identified in asbestos-induced MMs arising in Nf2 (+/-) mice.  Array CGH analysis was used to detect a recurrent deletion at chromosome 4C6.  A candidate in this region, Faf1 (FAS-associated factor 1), was further explored because it encodes a protein implicated in tumor cell survival and in the pathogenesis of some human tumor types.  We confirmed hemizygous loss of Faf1 and down regulation of Faf1 protein in a series of MMs from Arf (+/-) mice, and then showed that Faf1 regulates TNFalpha-mediated NFkappaB signaling, a mechanism previously implicated in asbestos-induced oncogenesis of human mesothelial cells.  Collectively, these investigations divulge important information regarding the significance of Arf inactivation in MM pathogenesis, and implicate Faf1 as a key component in the TNFalpha/NFkappaB signaling node that has now been independently implicated in the asbestos-induced oncogenesis."
GSE12421_series_matrix.txtimp_info.txt
OBF r is 2 
Found overexpression in !Series_title	"Analysis of OBF-1 overexpression in early B cells"
GSE12421_series_matrix.txtimp_info.txt
OBF-1 r is 2 
Found overexpression in !Series_title	"Analysis of OBF-1 overexpression in early B cells"
GSE12425_series_matrix.txtimp_info.txt
Notch4 r is 1 
Found overexpression in !Series_title	"Dox-regulated Notch4 overexpression in mouse ES cells redirects hemagioblasts to a cardiac fate."
GSE12425_series_matrix.txtimp_info.txt
Flk-1 r is 7 
Found stimulation in !Series_summary	"To investigate the role of Notch signalling in the establishment of cardiac lineages, we used a tet-inducible ES cell line (Ainv18) engineered to express an activated form of the Notch4 receptor following doxycycline treatment. This line also expresses a GFP cDNA from the Bry locus. Following 3.0-3.5 days of serum stimulation, three distinct populations based on Flk-1 and GFP expression are observed: Bry-GFP-/Flk-1-, Bry-GFP+/Flk-1- and Bry-GFP+/Flk-1+ cells.  Previous studies have shown that the Bry-GFP+/Flk-1+ population contains hemangioblasts, whereas the Bry-GFP+/Flk-1- population displays cardiac potential."
GSE12430_series_matrix.txtimp_info.txt
Math1 r is 8 
Found knockout in !Series_summary	"Cells from 5 GFAP-Cre tumors, 5 Math1-Cre tumors, and 5 conventional patched-knockout tumors will be isolated using enzymatic digestion and Percoll gradient centrifugation. These procedures have been found to result in 85-95% pure tumor cell populations. In addition, 5 tumors will be FACS-sorted to isolate CD15+ and CD15- populations. RNA will be prepared from each of these samples using an RNeasy kit from Qiagen. Samples of 2 micrograms will be resuspended in 10 microliters of RNase-free water, and sent to the Consortium for labeling, hybridization and analysis. Cells from the three types of tumors, and CD15+ and CD15- cells,  will be compared to one another."
GSE12441_series_matrix.txtimp_info.txt
Wnt3a r is 3 
Found treated in !Series_overall_design	"Cells derived from mouse embryonic stage 11.5 limb buds were cultured and treated with purified Wnt3a protein or vehicle controls. The transcriptional response was detected using spotted cDNA microarrays after 2 hrs or 4 hrs of treatment. 4 biological replicates were used per condition."
GSE12454_series_matrix.txtimp_info.txt
Atrx r is 1 
Found null in !Series_overall_design	"At P0.5, n = 4 biological replicates of littermate-matched wt/ko pairs (for pair #2 there is one wt and 2 Atrx-null samples (2A & 2B) and we count this as 2 pairs)."
GSE12464_series_matrix.txtimp_info.txt
Itk r is 1 
Found knockout in !Series_overall_design	"CD3+ T-cells from pooled suspensions of spleen and lymph nodes of Wt and Itk knockout mice on C57BL/6 background were isolated after negative depletion. Unstimulated as well as stimulated T-cells were studied. Stimulations were done with anti-CD3 (1 mg/ml) with or without anti-CD28 (3 mg/ml) in the presence or absence of CsA (1 mg/ml) for 24 hrs. For each stimulus, at least duplicate samples were used."
GSE12464_series_matrix.txtimp_info.txt
Itk r is 8 
Found activation in !Series_summary	"The Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays. The largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found. Taken together, our study provides a general overview about the global transcriptional changes in the absence of Itk."
GSE12464_series_matrix.txtimp_info.txt
CD3 r is 1 
Found stimulation in !Series_summary	"The Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays. The largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found. Taken together, our study provides a general overview about the global transcriptional changes in the absence of Itk."
GSE12465_series_matrix.txtimp_info.txt
Itk r is 1 
Found knockout in !Series_overall_design	"CD3+ CD4+ and CD8+ T-cells from pooled suspensions of spleen and lymph nodes of Wt and Itk knockout mice on C57BL/6 background were isolated after negative depletion. Unstimulated as well as stimulated T-cells were studied. Stimulations were done with anti-CD3 (1 mg/ml) for 24 hrs. For the CD4+ T-cells we collected triplicates from the Itk knockout mice and duplicates from the Wt group. For the CD8+ T-cells, we got duplicates from Itk knockout , while we obtained a single sample from Wt owing to the low cell yield for resting Wt CD8+ T-cells. After CD3-stimulation we got a single sample from the CD8+ subset of both Wt and Itk knockout, while for the CD4+ subsets we collected duplicates."
GSE12465_series_matrix.txtimp_info.txt
Itk r is 8 
Found activation in !Series_summary	"The Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays. The largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found. Taken together, our study provides a general overview about the global transcriptional changes in the absence of Itk."
GSE12465_series_matrix.txtimp_info.txt
CD3 r is 1 
Found stimulation in !Series_summary	"The Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays. The largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found. Taken together, our study provides a general overview about the global transcriptional changes in the absence of Itk."
GSE12466_series_matrix.txtimp_info.txt
Itk r is 1 
Found deficient in !Series_title	"Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells"
GSE12467_series_matrix.txtimp_info.txt
Myc r is 2 
Found loss of in !Series_summary	"Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs. "
GSE12467_series_matrix.txtimp_info.txt
LT r is 1 
Found deficient in !Series_title	"Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs"
GSE12467_series_matrix.txtimp_info.txt
N-myc r is 2 
Found deficient in !Series_title	"Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs"
GSE12467_series_matrix.txtimp_info.txt
N-myc r is 2 
Found deficient in !Series_summary	"Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs. "
GSE12489_series_matrix.txtimp_info.txt
PXR r is 3 
Found -/- in !Series_overall_design	"Animals were injected i.p. 100mg/kg phenobarbital or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the phenobarbital treated ones and hybridized to Sterolgene V1 arrays."
GSE12489_series_matrix.txtimp_info.txt
V1 r is 6 
Found treated in !Series_overall_design	"Animals were injected i.p. 100mg/kg phenobarbital or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the phenobarbital treated ones and hybridized to Sterolgene V1 arrays."
GSE12495_series_matrix.txtimp_info.txt
Trsp r is 4 
Found knockout in !Series_title	"Wild type mice (Trsp) vs Trsp-knockout mice (DTrsp) or A34 or G37L or G37H transgenic mice"
GSE12495_series_matrix.txtimp_info.txt
Trsp r is 1 
Found knockout in !Series_summary	"Comparative analysis of gene expression in the liver of the Trsp-knockout mice  (Trspfl/fl-AlbCre+/+) and A34 (Trspfl/fl-AlbCre+/+-A34t/t), G37L (Trspfl/fl-AlbCre+/+-G37t/t; 2 copies), G37H (Trspfl/fl-AlbCre+/+-G37t/t; 16 copies) transgenic mice with gene expression of wild type mice (Trsp+/+-AlbCre+/+)."
GSE12495_series_matrix.txtimp_info.txt
selenoprotein r is 5 
Found mutant in !Series_summary	"Sec (selenocysteine) is biosynthesized on its tRNA and incorporated into selenium-containing proteins (selenoproteins) as the 21st amino acid residue. Selenoprotein synthesis is dependent on Sec tRNA and the expression of this class of proteins can be modulated by altering Sec tRNA expression. The gene encoding Sec tRNA (Trsp) is a single-copy gene and its targeted removal in liver demonstrated that selenoproteins are essential for proper function wherein their absence leads to necrosis and hepatocellular degeneration. In the present study, we found that the complete loss of selenoproteins in liver was compensated for by an enhanced expression of several phase II response genes and their corresponding gene products. The replacement of selenoprotein synthesis in mice carrying mutant Trsp transgenes, wherein housekeeping, but not stress-related selenoproteins are expressed, led to normal expression of phase II response genes. Thus the present study provides evidence for a functional link between housekeeping selenoproteins and phase II enzymes."
GSE12498_series_matrix.txtimp_info.txt
EMT r is 7 
Found inhibition in !Series_summary	"Regulation of organ size is important for development and tissue homeostasis. In  Drosophila, Hippo signaling controls organ size by regulating the activity of a TEAD  transcription factor, Scalloped, through modulation of its coactivator protein Yki. The  role of mammalian Tead proteins in growth regulation, however, remains unknown.  Here we examined the role of mouse Tead proteins in growth regulation. In NIH3T3  cells, cell density and Hippo signaling regulated the activity of Tead proteins by  modulating nuclear localization of a Yki homologue, Yap, and the resulting change in  Tead activity altered cell proliferation. Tead2-VP16 mimicked Yap overexpression,  including increased cell proliferation, reduced cell death, promotion of EMT, lack of cell  contact inhibition, and promotion of tumor formation. Growth promoting activities of  various Yap mutants correlated with their Tead-coactivator activities. Tead2-VP16 and  Yap regulated largely overlapping sets of genes. However, only a few of the Tead/Yapregulated  genes in NIH3T3 cells were affected in Tead1-/-;Tead2-/- or Yap-/- embryos. Most  of the previously identified Yap-regulated genes were not affected in NIH3T3 cells or  mutant mice. In embryos, levels of nuclear Yap and Tead1 varied depending on cell  types. Strong nuclear accumulation of Yap and Tead1 were seen in myocardium,  correlating with requirements of Tead1 for proliferation. However, their distribution did  not always correlate with proliferation. Taken together, mammalian Tead proteins  regulate cell proliferation and contact inhibition as a transcriptional mediator of Hippo  signaling, but the mechanisms by which Tead/Yap regulate cell proliferation differ  depending on cell types, and Tead, Yap and Hippo signaling may play multiple roles in  mouse embryos."
GSE12498_series_matrix.txtimp_info.txt
Tead1 r is 1 
Found -/- in !Series_summary	"Regulation of organ size is important for development and tissue homeostasis. In  Drosophila, Hippo signaling controls organ size by regulating the activity of a TEAD  transcription factor, Scalloped, through modulation of its coactivator protein Yki. The  role of mammalian Tead proteins in growth regulation, however, remains unknown.  Here we examined the role of mouse Tead proteins in growth regulation. In NIH3T3  cells, cell density and Hippo signaling regulated the activity of Tead proteins by  modulating nuclear localization of a Yki homologue, Yap, and the resulting change in  Tead activity altered cell proliferation. Tead2-VP16 mimicked Yap overexpression,  including increased cell proliferation, reduced cell death, promotion of EMT, lack of cell  contact inhibition, and promotion of tumor formation. Growth promoting activities of  various Yap mutants correlated with their Tead-coactivator activities. Tead2-VP16 and  Yap regulated largely overlapping sets of genes. However, only a few of the Tead/Yapregulated  genes in NIH3T3 cells were affected in Tead1-/-;Tead2-/- or Yap-/- embryos. Most  of the previously identified Yap-regulated genes were not affected in NIH3T3 cells or  mutant mice. In embryos, levels of nuclear Yap and Tead1 varied depending on cell  types. Strong nuclear accumulation of Yap and Tead1 were seen in myocardium,  correlating with requirements of Tead1 for proliferation. However, their distribution did  not always correlate with proliferation. Taken together, mammalian Tead proteins  regulate cell proliferation and contact inhibition as a transcriptional mediator of Hippo  signaling, but the mechanisms by which Tead/Yap regulate cell proliferation differ  depending on cell types, and Tead, Yap and Hippo signaling may play multiple roles in  mouse embryos."
GSE12498_series_matrix.txtimp_info.txt
Yap r is 5 
Found expressing in !Series_overall_design	"Tead2-VP16-, Tead2-EnR-, Yap- and control vector-expressing cells were cultured at low or high density for RNA extraction and hybridization on Affymetrix microarrays."
GSE12498_series_matrix.txtimp_info.txt
Tead2 r is 4 
Found overexpression in !Series_summary	"Regulation of organ size is important for development and tissue homeostasis. In  Drosophila, Hippo signaling controls organ size by regulating the activity of a TEAD  transcription factor, Scalloped, through modulation of its coactivator protein Yki. The  role of mammalian Tead proteins in growth regulation, however, remains unknown.  Here we examined the role of mouse Tead proteins in growth regulation. In NIH3T3  cells, cell density and Hippo signaling regulated the activity of Tead proteins by  modulating nuclear localization of a Yki homologue, Yap, and the resulting change in  Tead activity altered cell proliferation. Tead2-VP16 mimicked Yap overexpression,  including increased cell proliferation, reduced cell death, promotion of EMT, lack of cell  contact inhibition, and promotion of tumor formation. Growth promoting activities of  various Yap mutants correlated with their Tead-coactivator activities. Tead2-VP16 and  Yap regulated largely overlapping sets of genes. However, only a few of the Tead/Yapregulated  genes in NIH3T3 cells were affected in Tead1-/-;Tead2-/- or Yap-/- embryos. Most  of the previously identified Yap-regulated genes were not affected in NIH3T3 cells or  mutant mice. In embryos, levels of nuclear Yap and Tead1 varied depending on cell  types. Strong nuclear accumulation of Yap and Tead1 were seen in myocardium,  correlating with requirements of Tead1 for proliferation. However, their distribution did  not always correlate with proliferation. Taken together, mammalian Tead proteins  regulate cell proliferation and contact inhibition as a transcriptional mediator of Hippo  signaling, but the mechanisms by which Tead/Yap regulate cell proliferation differ  depending on cell types, and Tead, Yap and Hippo signaling may play multiple roles in  mouse embryos."
GSE12503_series_matrix.txtimp_info.txt
Agr2 r is 1 
Found -/- in !Series_summary	"Keywords: small intestine and colon gene expression profiles for Agr2-/- and littermate control mice"
GSE12506_series_matrix.txtimp_info.txt
Ag r is 4 
Found induced in !Series_overall_design	"To define the molecular signature of Ag-specific in vivo-induced dtg CD25 TR cells in comparison to naturally occurring CD25 TR cells, we performed comparative gene expression profiling by Affymetrix microarray analysis. Sorted splenic wild-type (WT) TR cells, stg TR cells, dtg CD25-  TR cells, dtg CD25+  TR cells, in vitro-stimulated stg 16h TA cells, stg 3d TA cells as well as stg TN cells, were included in the experiment and analyses were performed in triplicates."
GSE12506_series_matrix.txtimp_info.txt
TR r is 3 
Found induced in !Series_overall_design	"To define the molecular signature of Ag-specific in vivo-induced dtg CD25 TR cells in comparison to naturally occurring CD25 TR cells, we performed comparative gene expression profiling by Affymetrix microarray analysis. Sorted splenic wild-type (WT) TR cells, stg TR cells, dtg CD25-  TR cells, dtg CD25+  TR cells, in vitro-stimulated stg 16h TA cells, stg 3d TA cells as well as stg TN cells, were included in the experiment and analyses were performed in triplicates."
GSE12506_series_matrix.txtimp_info.txt
CD25 r is 2 
Found induced in !Series_overall_design	"To define the molecular signature of Ag-specific in vivo-induced dtg CD25 TR cells in comparison to naturally occurring CD25 TR cells, we performed comparative gene expression profiling by Affymetrix microarray analysis. Sorted splenic wild-type (WT) TR cells, stg TR cells, dtg CD25-  TR cells, dtg CD25+  TR cells, in vitro-stimulated stg 16h TA cells, stg 3d TA cells as well as stg TN cells, were included in the experiment and analyses were performed in triplicates."
GSE12509_series_matrix.txtimp_info.txt
PXR r is 3 
Found -/- in !Series_overall_design	"Animals were injected i.p. 10mg/kg TCPOBOP or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the TCPOBOP treated ones and hybridized to Sterolgene V1 arrays."
GSE12509_series_matrix.txtimp_info.txt
V1 r is 6 
Found treated in !Series_overall_design	"Animals were injected i.p. 10mg/kg TCPOBOP or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the TCPOBOP treated ones and hybridized to Sterolgene V1 arrays."
GSE12536_series_matrix.txtimp_info.txt
Myc r is 2 
Found loss of in !Series_summary	"Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs and commited progenitors."
GSE12536_series_matrix.txtimp_info.txt
N-myc r is 2 
Found deficient in !Series_title	"Differentially regulated genes in control and c-myc N-myc deficient progenitors"
GSE12536_series_matrix.txtimp_info.txt
N-myc r is 2 
Found deficient in !Series_summary	"Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs and commited progenitors."
GSE12537_series_matrix.txtimp_info.txt
PXR r is 3 
Found -/- in !Series_overall_design	"Animals were injected i.p. 40mg/kg PCN or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the PCN treated ones and hybridized to Steroltalk V2 arrays."
GSE12538_series_matrix.txtimp_info.txt
LT r is 1 
Found deficient in !Series_title	"Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs and progenitors"
GSE12538_series_matrix.txtimp_info.txt
N-myc r is 2 
Found deficient in !Series_title	"Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs and progenitors"
GSE12541-GPL2872_series_matrix.txtimp_info.txt
Aoh2 r is 2 
Found knockout in !Series_title	"Aldehyde oxidase homologue 2 (Aoh2) knockout mouse and retinoic acid synthesis"
GSE12541-GPL7202_series_matrix.txtimp_info.txt
Aoh2 r is 2 
Found knockout in !Series_title	"Aldehyde oxidase homologue 2 (Aoh2) knockout mouse and retinoic acid synthesis"
GSE12545_series_matrix.txtimp_info.txt
Gfi1 r is 1 
Found -/- in !Series_title	"Global gene expression analysis between Gfi1+/+ and Gfi1-/- splenic B cells"
GSE12545_series_matrix.txtimp_info.txt
Gfi1 r is 1 
Found -/- in !Series_overall_design	"Splenic B220+CD19+ CD138- B cells of 4 week old Gfi1+/+ and Gfi1-/- mice were isolated and RNA was extracted from one sample per group and microarray analysis was performed."
GSE12576_series_matrix.txtimp_info.txt
PrP r is 1 
Found null in !Series_overall_design	"Wild type (WT), PrP-null (KO), and Tg(HQK) mice were fed food pellets either lacking or containing 6g doxycycline (Dox)/kg food to induce PrPC expression. Skeletal muscles from the quadriceps of hind legs were removed at day 0, 4, 7, 14, 30 and 60 days following administration of Dox.  Total RNA was isolated from these tissues for use in subsequent microarray analysis. Mouse gene expression was analysed by two-colour microarray experiments using an inhouse manufactured 16K mouse cDNA microarray. Age matched reference mice (WT) and experimental (KO and HQK) Alexa Flour labeled aRNA were used in each competitive hybridization.  Each sample was labeled individually with both Alexa Fluor 555 and 647 for subsequent dye-swapped hybridizations to account for intensity bias. 3 individual mice from each experimental group at each time point were individually processed for separate microarrays.  We used the program EDGE to identify genes that were differentially expressed in mouse skeletal muscle in either transgenic HQK mice over expressing PrP, or PrP knock out (KO) mice  after administration of Dox.  We used a P value cut-off of 0.05 as the criteria of selection of significantly differentially expressed genes."
GSE12576_series_matrix.txtimp_info.txt
Tg r is 6 
Found null in !Series_overall_design	"Wild type (WT), PrP-null (KO), and Tg(HQK) mice were fed food pellets either lacking or containing 6g doxycycline (Dox)/kg food to induce PrPC expression. Skeletal muscles from the quadriceps of hind legs were removed at day 0, 4, 7, 14, 30 and 60 days following administration of Dox.  Total RNA was isolated from these tissues for use in subsequent microarray analysis. Mouse gene expression was analysed by two-colour microarray experiments using an inhouse manufactured 16K mouse cDNA microarray. Age matched reference mice (WT) and experimental (KO and HQK) Alexa Flour labeled aRNA were used in each competitive hybridization.  Each sample was labeled individually with both Alexa Fluor 555 and 647 for subsequent dye-swapped hybridizations to account for intensity bias. 3 individual mice from each experimental group at each time point were individually processed for separate microarrays.  We used the program EDGE to identify genes that were differentially expressed in mouse skeletal muscle in either transgenic HQK mice over expressing PrP, or PrP knock out (KO) mice  after administration of Dox.  We used a P value cut-off of 0.05 as the criteria of selection of significantly differentially expressed genes."
GSE12576_series_matrix.txtimp_info.txt
PrP r is 3 
Found KO in !Series_overall_design	"Wild type (WT), PrP-null (KO), and Tg(HQK) mice were fed food pellets either lacking or containing 6g doxycycline (Dox)/kg food to induce PrPC expression. Skeletal muscles from the quadriceps of hind legs were removed at day 0, 4, 7, 14, 30 and 60 days following administration of Dox.  Total RNA was isolated from these tissues for use in subsequent microarray analysis. Mouse gene expression was analysed by two-colour microarray experiments using an inhouse manufactured 16K mouse cDNA microarray. Age matched reference mice (WT) and experimental (KO and HQK) Alexa Flour labeled aRNA were used in each competitive hybridization.  Each sample was labeled individually with both Alexa Fluor 555 and 647 for subsequent dye-swapped hybridizations to account for intensity bias. 3 individual mice from each experimental group at each time point were individually processed for separate microarrays.  We used the program EDGE to identify genes that were differentially expressed in mouse skeletal muscle in either transgenic HQK mice over expressing PrP, or PrP knock out (KO) mice  after administration of Dox.  We used a P value cut-off of 0.05 as the criteria of selection of significantly differentially expressed genes."
GSE12576_series_matrix.txtimp_info.txt
Tg r is 4 
Found KO in !Series_overall_design	"Wild type (WT), PrP-null (KO), and Tg(HQK) mice were fed food pellets either lacking or containing 6g doxycycline (Dox)/kg food to induce PrPC expression. Skeletal muscles from the quadriceps of hind legs were removed at day 0, 4, 7, 14, 30 and 60 days following administration of Dox.  Total RNA was isolated from these tissues for use in subsequent microarray analysis. Mouse gene expression was analysed by two-colour microarray experiments using an inhouse manufactured 16K mouse cDNA microarray. Age matched reference mice (WT) and experimental (KO and HQK) Alexa Flour labeled aRNA were used in each competitive hybridization.  Each sample was labeled individually with both Alexa Fluor 555 and 647 for subsequent dye-swapped hybridizations to account for intensity bias. 3 individual mice from each experimental group at each time point were individually processed for separate microarrays.  We used the program EDGE to identify genes that were differentially expressed in mouse skeletal muscle in either transgenic HQK mice over expressing PrP, or PrP knock out (KO) mice  after administration of Dox.  We used a P value cut-off of 0.05 as the criteria of selection of significantly differentially expressed genes."
GSE12609_series_matrix.txtimp_info.txt
Arx r is 1 
Found null in !Series_title	"Transcription factor Arx null brains (fulp-affy-mouse-364520)"
GSE12637_series_matrix.txtimp_info.txt
ras r is 1 
Found -/- in !Series_summary	"This experiment is to identify genes that are regulated by pRb in AC61 cells. AC61 cells were derived from a C-cell adenocarcinoma developed in an Rb+/-N-ras-/- mouse. "
GSE12637_series_matrix.txtimp_info.txt
N-ras r is 2 
Found -/- in !Series_summary	"This experiment is to identify genes that are regulated by pRb in AC61 cells. AC61 cells were derived from a C-cell adenocarcinoma developed in an Rb+/-N-ras-/- mouse. "
GSE12673_series_matrix.txtimp_info.txt
alpha-MHC r is 5 
Found expressing in !Series_overall_design	"Bi-allelic transgenic mice were created by crossing alpha-MHC promoter/tet transactivating protein expressing mice with tet responsive element promter/stable HIF-1alpha protein expressing mice.  Mice were either, maintained on Doxycycline (inhibiting the expression of the HIF-1alpha transgene) or removed from doxycycline (inducing expression) for one or three days."
GSE12687_series_matrix.txtimp_info.txt
GAP-43 r is 4 
Found KO in !Series_summary	"Mice lacking the growth associated protein, GAP-43, (KO) show multiple deficits in forebrain axon guidance and cortical cell differentiation (Donovan and McCasland, 2005). As a result, GAP-43 KO mice fail to form barrels in mouse somatosensory cortex (S1) (Maier et al., 1999). GAP-43 heterozygous (HZ) mice show abnormalities in axonal pathfinding and show larger than normal barrels in layer IV S1 due to widely branched thalamocortical afferents (TCAs). Regardless of abnormalities during early development, HZ barrels become indistinguishable from WT by postnatal day 26. One explanation for these findings is that compensatory mechanisms may be activated in GAP-43 HZ cortex. We have used mRNA microarray expression analysis to gain a more comprehensive view of genes involved in GAP-43 signaling during barrel map formation. Using laser  microdissection , cortical cells of the barrel cortex were excised, RNA extracted and used in GeneChip analysis. Expression profiling and functional gene group analysis of RNA from WT, HZ, and KO cortex at postnatal day 5 was performed. We identified thousands of transcripts differentially expressed across the genotypes. Verification of selected changes in gene expression was accomplished using in situ hybridization. Our results suggest an adaptive modification in transcript expression of genes involved in cell-cell communication and synaptogenesis. These modifications appear important in forward and reverse signaling as well as maintaining synchrony between the cells. Compensatory up- and down regulation of synapse-associated genes may explain the reverse in HZ phenotype from P7 to P26. Moreover, these findings provide new insight into the role GAP-43 plays in several pathways associated with synaptogenesis and trans-synaptic signaling."
GSE12687_series_matrix.txtimp_info.txt
GAP-43 r is 6 
Found lacking in !Series_summary	"Mice lacking the growth associated protein, GAP-43, (KO) show multiple deficits in forebrain axon guidance and cortical cell differentiation (Donovan and McCasland, 2005). As a result, GAP-43 KO mice fail to form barrels in mouse somatosensory cortex (S1) (Maier et al., 1999). GAP-43 heterozygous (HZ) mice show abnormalities in axonal pathfinding and show larger than normal barrels in layer IV S1 due to widely branched thalamocortical afferents (TCAs). Regardless of abnormalities during early development, HZ barrels become indistinguishable from WT by postnatal day 26. One explanation for these findings is that compensatory mechanisms may be activated in GAP-43 HZ cortex. We have used mRNA microarray expression analysis to gain a more comprehensive view of genes involved in GAP-43 signaling during barrel map formation. Using laser  microdissection , cortical cells of the barrel cortex were excised, RNA extracted and used in GeneChip analysis. Expression profiling and functional gene group analysis of RNA from WT, HZ, and KO cortex at postnatal day 5 was performed. We identified thousands of transcripts differentially expressed across the genotypes. Verification of selected changes in gene expression was accomplished using in situ hybridization. Our results suggest an adaptive modification in transcript expression of genes involved in cell-cell communication and synaptogenesis. These modifications appear important in forward and reverse signaling as well as maintaining synchrony between the cells. Compensatory up- and down regulation of synapse-associated genes may explain the reverse in HZ phenotype from P7 to P26. Moreover, these findings provide new insight into the role GAP-43 plays in several pathways associated with synaptogenesis and trans-synaptic signaling."
GSE12694_series_matrix.txtimp_info.txt
Pten r is 4 
Found deletion in !Series_summary	"Glioblastoma (GBM) is a highly lethal brain tumor presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM subtype presents acutely as high-grade disease that typically harbors EGFR, PTEN and Ink4a/Arf mutations, and the secondary GBM subtype evolves from the slow progression of low-grade disease that classically possesses PDGF and p53 events1.  Here, we show that concomitant CNS-specific deletion of p53 and Pten in the mouse CNS generates a penetrant acute-onset high-grade malignant glioma phenotype with striking clinical, pathological and molecular resemblance to primary GBM in humans.  This genetic observation prompted p53 and PTEN mutational analysis in human primary GBM, demonstrating unexpectedly frequent inactivating mutations of p53 as well the expected PTEN mutations.  Integrated transcriptomic profling, in silico promoter analysis and functional studies of murine neural stem cells (NSCs) established that dual, but not singular, inactivation of p53 and Pten promotes an undifferentiated state with high renewal potential and drives elevated c-Myc levels and its associated signature.  Functional studies validated increased c-Myc activity as a potent contributor to the impaired differentiation and enhanced renewal of p53-Pten null NSCs as well as tumor neurospheres (TNSs) derived from this model.  c-Myc also serves to maintain robust tumorigenic potential of p53-Pten null TNSs. These murine modeling studies, together with confirmatory transcriptomic/promoter studies in human primary GBM, validate a pathogenetic role of a common tumor suppressor mutation profile in human primary GBM and establish c-Myc as a key target for cooperative actions of p53 and Pten in the regulation of normal and malignant stem/progenitor cell differentiation, self-renewal and tumorigenic potential."
GSE12694_series_matrix.txtimp_info.txt
p53 r is 1 
Found null in !Series_summary	"We used microarrays to detail the gene expression difference of the p53-null and p53/Pten-doubly null neural stem cell after differentiation ."
GSE12694_series_matrix.txtimp_info.txt
p53 r is 1 
Found null in !Series_overall_design	"transcriptome comparisons of 2 independent p53-null with 3 p53/Pten double-null murine NSCs at 1 day post exposure to the differentiation inducer."
GSE12697_series_matrix.txtimp_info.txt
TNF-alpha r is 2 
Found induced in !Series_title	"Trap-80-dependence of TNF-alpha-induced genes"
GSE12697_series_matrix.txtimp_info.txt
TNF-alpha r is 7 
Found stimulated in !Series_overall_design	"RNA was extracted from three independent cultures of wild-type and Trap-80 knock-down fibroblasts, before and after stimulation for 1 hour with 5ng/ml TNF-alpha.  The unstimulated and stimulated wild-type samples, and the stimulated Trap-80 knock-down samples, were used for microarray analysis."
GSE12697_series_matrix.txtimp_info.txt
NF r is 2 
Found stimulation in !Series_summary	"In fibroblasts, p65-dependent genes can be sub-divided, depending on whether they are Trap-80-dependent or -independent.  To examine the generality of this grouping, we performed a microarray analysis of wild-type and Trap-80 knock-down fibroblasts, before and after stimulation of NF-kappaB activity using TNF-alpha."
GSE12697_series_matrix.txtimp_info.txt
NF-kappaB r is 2 
Found stimulation in !Series_summary	"In fibroblasts, p65-dependent genes can be sub-divided, depending on whether they are Trap-80-dependent or -independent.  To examine the generality of this grouping, we performed a microarray analysis of wild-type and Trap-80 knock-down fibroblasts, before and after stimulation of NF-kappaB activity using TNF-alpha."
GSE12697_series_matrix.txtimp_info.txt
TNF-alpha r is 6 
Found stimulation in !Series_summary	"In fibroblasts, p65-dependent genes can be sub-divided, depending on whether they are Trap-80-dependent or -independent.  To examine the generality of this grouping, we performed a microarray analysis of wild-type and Trap-80 knock-down fibroblasts, before and after stimulation of NF-kappaB activity using TNF-alpha."
GSE12697_series_matrix.txtimp_info.txt
TNF-alpha r is 6 
Found stimulation in !Series_overall_design	"RNA was extracted from three independent cultures of wild-type and Trap-80 knock-down fibroblasts, before and after stimulation for 1 hour with 5ng/ml TNF-alpha.  The unstimulated and stimulated wild-type samples, and the stimulated Trap-80 knock-down samples, were used for microarray analysis."
GSE12707_series_matrix.txtimp_info.txt
Atg16l1 r is 1 
Found mutant in !Series_summary	"The aim of this study is to survey global gene expression of total thymocytes from wild-type mice and Atg16l1 mutant (hypomorph) mice."
GSE12712_series_matrix.txtimp_info.txt
rsl r is 1 
Found null in !Series_overall_design	"Total RNA was extracted from livers of adult male and female wild type, rsl-null and transgenic mice that overexpress Rsl1 or Rsl2, specifically in the liver. Equivalent amounts of RNA were pooled from five or more mice per sex and genotype. Two pools per sex and genotype were hybridized to the Affymetrix Mouse Genome 430 2.0 array."
GSE12712_series_matrix.txtimp_info.txt
Rsl1 r is 6 
Found null in !Series_overall_design	"Total RNA was extracted from livers of adult male and female wild type, rsl-null and transgenic mice that overexpress Rsl1 or Rsl2, specifically in the liver. Equivalent amounts of RNA were pooled from five or more mice per sex and genotype. Two pools per sex and genotype were hybridized to the Affymetrix Mouse Genome 430 2.0 array."
GSE12712_series_matrix.txtimp_info.txt
Rsl2 r is 8 
Found null in !Series_overall_design	"Total RNA was extracted from livers of adult male and female wild type, rsl-null and transgenic mice that overexpress Rsl1 or Rsl2, specifically in the liver. Equivalent amounts of RNA were pooled from five or more mice per sex and genotype. Two pools per sex and genotype were hybridized to the Affymetrix Mouse Genome 430 2.0 array."
GSE12753_series_matrix.txtimp_info.txt
Tg r is 5 
Found -/- in !Series_overall_design	"We established ES cell lines with four different genotypes for Rex1; ES cells carrying the wild-type Rex1 alleles and the empty CAG-IZ vector (wt), the wild-type Rex1 alleles and the Rex1 transgene (wt-Tg), the Rex1-/- alleles and the empty vector(KO), and the Rex1-/- alleles and the Rex1 transgene (KO-Tg). The genetically-engineered ES cell lines were generated to analyze the function of Rex1 in the maintenance of pluripotency and to analyze its gain- and loss-of function. For loss-of-function analysis, we disrupted the endogenous Rex1 allele by conventional gene targeting via homologous recombination in ES cells. The knock-out (KO) allele should be a functionally null allele because the first 100 bp of the open reading frame in the exon 4 including the start codon was replaced by the pacEGFP chimeric gene cassette containing the puromycin-resistant gene (pac) and the green fluorescent protein (Egfp) cDNA. Interestingly, all of the puromycin resistant clones obtained by transfection of this KO vector carried the correctly targeted alleles. One of the Rex1+/- ES cell line (RKPG9) was cultured with high-dose puromycin to obtain the Rex1-/- ES cell lines generated via spontaneous gene conversion. Multiple Rex1-/- ES cell lines were established with extremely high efficiency (4 of 4 clones obtained after the selection were homozygous for Rex1 KO allele). Correct targeting events were confirmed by the loss of the polymorphic signature of the wild-type allele on the southern blot analysis of the genomic DNA, in which the 5.6 kb fragment corresponds to the Rex1 pseudogene on chromosome 15 reported previously as well as found in the mouse genome data. Northern blot revealed the loss of the transcript derived from the wild-type allele in Rex1-/- ES cells, which express the large transcripts composed by the truncated Rex1 and pacEGFP. Rex1-/- ES cells were also established by introduction of the second knockout vector carrying the hygromycin-resistant gene as a selection marker."
GSE12753_series_matrix.txtimp_info.txt
Rex1 r is 1 
Found -/- in !Series_overall_design	"Rex1+/- ES cell line (RKPG9), Rex1-/- ES cells (HP3 and HP4), and one wild-type ES cells (EB5)"
GSE12836_series_matrix.txtimp_info.txt
PDGF-B r is 2 
Found overexpression in !Series_summary	"We analyzed the generation of mouse gliomas following the overexpression of PDGF-B in embryonic neural progenitors. Comparison of our microarray data, with published gene expression data sets for many different murine neural cell types, revealed a closest relationship between our tumor cells and oligodendrocyte progenitor cells, confirming definitively that PDGF-B-induced gliomas are pure oligodendrogliomas."
GSE12863_series_matrix.txtimp_info.txt
Ets2 r is 8 
Found deficient in !Series_overall_design	"Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling."
GSE12863_series_matrix.txtimp_info.txt
Ets2 r is 4 
Found induced in !Series_overall_design	"Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling."
GSE12863_series_matrix.txtimp_info.txt
Ets2 r is 1 
Found expressing in !Series_overall_design	"Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling."
GSE12867_series_matrix.txtimp_info.txt
Sun1 r is 1 
Found -/- in !Series_overall_design	"Total RNA was isolated from E14.5 mouse embryonic fibroblasts (MEFs) and and day 9 and 14 mouse whole testes.  cDNA samples from paired (same parents) wt (Cy3-labled) and Sun1-/- (Cy5-labled) mice were mixed and hybridized."
GSE12881_series_matrix.txtimp_info.txt
Cav r is 2 
Found knockout in !Series_overall_design	"All WT and Cav-3 knockout (KO) mice used in this study were in the FVB/N genetic background. 4-month old virgin female mice were utilized in a micro array study between 3 wildtype and 3 Caveolin-3 knock-out mammary glands."
GSE12881_series_matrix.txtimp_info.txt
Cav-3 r is 2 
Found knockout in !Series_overall_design	"All WT and Cav-3 knockout (KO) mice used in this study were in the FVB/N genetic background. 4-month old virgin female mice were utilized in a micro array study between 3 wildtype and 3 Caveolin-3 knock-out mammary glands."
GSE12881_series_matrix.txtimp_info.txt
Cav r is 4 
Found KO in !Series_overall_design	"All WT and Cav-3 knockout (KO) mice used in this study were in the FVB/N genetic background. 4-month old virgin female mice were utilized in a micro array study between 3 wildtype and 3 Caveolin-3 knock-out mammary glands."
GSE12881_series_matrix.txtimp_info.txt
Cav-3 r is 4 
Found KO in !Series_overall_design	"All WT and Cav-3 knockout (KO) mice used in this study were in the FVB/N genetic background. 4-month old virgin female mice were utilized in a micro array study between 3 wildtype and 3 Caveolin-3 knock-out mammary glands."
GSE12905_series_matrix.txtimp_info.txt
Foxl2 r is 1 
Found null in !Series_summary	"Comparison of Foxl2-null ovaries to wildtype ovaries, ovaries lacking Wnt4 or Kit, or testes, throughout mouse development."
GSE12905_series_matrix.txtimp_info.txt
Wnt4 r is 8 
Found null in !Series_summary	"Comparison of Foxl2-null ovaries to wildtype ovaries, ovaries lacking Wnt4 or Kit, or testes, throughout mouse development."
GSE12905_series_matrix.txtimp_info.txt
Kit r is 3 
Found lacking in !Series_summary	"Comparison of Foxl2-null ovaries to wildtype ovaries, ovaries lacking Wnt4 or Kit, or testes, throughout mouse development."
GSE12905_series_matrix.txtimp_info.txt
Foxl2 r is 8 
Found lacking in !Series_summary	"Comparison of Foxl2-null ovaries to wildtype ovaries, ovaries lacking Wnt4 or Kit, or testes, throughout mouse development."
GSE12905_series_matrix.txtimp_info.txt
Wnt4 r is 1 
Found lacking in !Series_summary	"Comparison of Foxl2-null ovaries to wildtype ovaries, ovaries lacking Wnt4 or Kit, or testes, throughout mouse development."
GSE12931_series_matrix.txtimp_info.txt
Kit r is 3 
Found mutant in !Series_title	"Murine model of gastrointestinal stromal tumors harboring a germline Kit K641E oncogenic mutant "
GSE12931_series_matrix.txtimp_info.txt
Kit r is 2 
Found mutant in !Series_summary	"Gastrointestinal stromal tumors (GIST) are thought to derive from the interstitial cells of Cajal (ICC) or an ICC precursor. Oncogenic mutations of the receptor tyrosine kinase KIT are present in most GIST. KIT K642E was originally identified in sporadic GIST and later found in the germ line of a familial GIST. A mouse model of harboring a germline Kit K641E mutant was created to model familial GIST. The expression profile was investigated in the gastric antrum in the knock-in Kit K641E murine GIST model by microarray."
GSE12954_series_matrix.txtimp_info.txt
Dll1 r is 1 
Found mutant in !Series_title	"Expression Profiling of Dll1 mutant mouse line"
GSE12954_series_matrix.txtimp_info.txt
Dll1 r is 1 
Found mutant in !Series_overall_design	"Four organs (liver, spleen, thymus, brain) of the Dll1 mutant mouse line analysed by cDNA microarray technology. Experiments include four biological replicates for reference (wildtype) and mutant animals. Two technical replicates for each mutant mouse were performed. As reference pooled RNA of the same organ was used. 50% of the chip hybridisations are dye sway experiments."
GSE12965-GPL6193_series_matrix.txtimp_info.txt
Nova2 r is 1 
Found KO in !Series_title	"Wild type vs. Nova2 KO mouse P10 cortex RNA"
GSE12965-GPL8940_series_matrix.txtimp_info.txt
Nova2 r is 1 
Found KO in !Series_title	"Wild type vs. Nova2 KO mouse P10 cortex RNA"
GSE12982_series_matrix.txtimp_info.txt
polycomb r is 2 
Found loss of in !Series_overall_design	"To assay the global effects of the loss of polycomb proteins (Ezh2 or Eed) in embryonic stem (ES) cells , we compared the expression profiles of homologuous Ezh2 or Eed knockout ES cells to wild-type ES cells in undifferentiated or differentiated condition."
GSE12982_series_matrix.txtimp_info.txt
Eed r is 7 
Found loss of in !Series_overall_design	"To assay the global effects of the loss of polycomb proteins (Ezh2 or Eed) in embryonic stem (ES) cells , we compared the expression profiles of homologuous Ezh2 or Eed knockout ES cells to wild-type ES cells in undifferentiated or differentiated condition."
GSE12982_series_matrix.txtimp_info.txt
Ezh2 r is 5 
Found loss of in !Series_overall_design	"To assay the global effects of the loss of polycomb proteins (Ezh2 or Eed) in embryonic stem (ES) cells , we compared the expression profiles of homologuous Ezh2 or Eed knockout ES cells to wild-type ES cells in undifferentiated or differentiated condition."
GSE13062_series_matrix.txtimp_info.txt
Cry1 r is 4 
Found KO in !Series_title	"The effects of temporally restricted feeding on hepatic gene expression of Cry1, Cry2 double KO mice"
GSE13062_series_matrix.txtimp_info.txt
Cry2 r is 2 
Found KO in !Series_title	"The effects of temporally restricted feeding on hepatic gene expression of Cry1, Cry2 double KO mice"
GSE13062_series_matrix.txtimp_info.txt
Cry1 r is 4 
Found KO in !Series_summary	"Restricted feeding impacts the hepatic circadian clock of WT mice. Cry1, Cry2 double KO mice lack a circadian clock and are thus expected to show rhythmical gene expression in the liver. Imposing a temporally restricted feeding schedule on these mice  shows how the hepatic circadian clock and rhythmic food intake regulate rhythmic transcription in parallel "
GSE13062_series_matrix.txtimp_info.txt
Cry2 r is 2 
Found KO in !Series_summary	"Restricted feeding impacts the hepatic circadian clock of WT mice. Cry1, Cry2 double KO mice lack a circadian clock and are thus expected to show rhythmical gene expression in the liver. Imposing a temporally restricted feeding schedule on these mice  shows how the hepatic circadian clock and rhythmic food intake regulate rhythmic transcription in parallel "
GSE13062_series_matrix.txtimp_info.txt
Cry2 r is 2 
Found KO in !Series_overall_design	"Cry1, Cry2 double KO mice were entrained either to ad libitum or temporally restricted feeding (tRF) schedules. Food was made available to mice under the tRF regimen only between ZT(CT)1 and ZT(CT)9. Mice were then released into constant darkness while the respective feeding schedules were still maintained. Liver tissue was collected on the second day of constant darkness at the indicated timepoints. Total RNA was extracted and 5ug of RNA was used in the standard Affymetrix protocol for amplification, labeling and hybridization"
GSE13071_series_matrix.txtimp_info.txt
CIA r is 3 
Found induced in !Series_title	"Knee joint synovium from different grades of inflammation in mouse collagen induced arthritis (CIA)"
GSE13071_series_matrix.txtimp_info.txt
CIA r is 3 
Found induced in !Series_summary	"Knee joint synovium was used for gene expression analysis of mouse collagen induced arthritis (CIA).  Synovium was prepared at day 30 after initial sensitization from: healthy controls, CIA animals with no, with mild, with moderate, or with severe joint inflammation.  Each sample group is represented by three replicates, each consisting of tissue collected from three to four animals."
GSE13129_series_matrix.txtimp_info.txt
F10 r is 6 
Found expressing in !Series_summary	"We wished to examine the genes regulated by FoxD3 in pigment cells to gain understanding in how FoxD3 represses melanoblast specification in the neural crest.  For technical reasons, we could not use neural crest cells, so we used melanoma cells, since they are derived from neural crest cells.  To this end, we transfected B16-F10 mouse melanoma cells with constructs expressing FoxD3, or FoxD3-VP16, in which the C-terminal portion of FoxD3 (which contains the transcriptional repression domain) has been replaced by the VP16 transcriptional activation domain."
GSE13130_series_matrix.txtimp_info.txt
aryl hydrocarbon receptor r is 3 
Found deficient in !Series_title	"Langerhans cells from aryl hydrocarbon receptor deficient mice"
GSE13140_series_matrix.txtimp_info.txt
DAP12 r is 4 
Found KO in !Series_title	"Basal and IL-4 response in DAP12 (TYROBP) KO mice"
GSE13140_series_matrix.txtimp_info.txt
DAP12 r is 1 
Found knockdown in !Series_overall_design	"The current experiment was designed to evaluate the effect of DAP12 knockdown on macrophage gene expression, both in basal conditions and in the response to IL-4."
GSE13140_series_matrix.txtimp_info.txt
DAP12 r is 6 
Found activation in !Series_summary	"DAP12 is a transmembrane protein, expressed as a disulfide-bonded homodimer and bears an immunoreceptor tyrosine-based activation motif (ITAM). DAP12 is broadly expressed in hematopoietic cells and associates with a variety of cell surface receptors in lymphoid and myeloid cells. Macrophages express several DAP12-associated receptors including triggering receptors expressed by myeloid cells (TREM)-1,2 and 3, myeloid DAP12-associating lectin (MDL)-1, CD200R like proteins CD200R3/R4 and CD300C/D/E ."
GSE13143_series_matrix.txtimp_info.txt
SMRT r is 2 
Found mutant in !Series_title	"Expression data from 3T3-MEFs derived from wild-type and SMRT RID mutant mice"
GSE13147_series_matrix.txtimp_info.txt
Trif r is 1 
Found -/- in !Series_summary	"Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila."
GSE13147_series_matrix.txtimp_info.txt
Myd88 r is 1 
Found -/- in !Series_summary	"Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila."
GSE13147_series_matrix.txtimp_info.txt
Trif r is 1 
Found -/- in !Series_overall_design	"Bone marrow-derived macrophages from Myd88-/-Trif-/- and Myd88-/-Rip2-/- mice were infected with WT L. pneumophila (Lp02) or dotA mutant L. pneumophila (Lp03) for 4 hours. The RNA was extracted, processed, and hybridized onto Affymetrix 430 2.0 microarrays"
GSE13147_series_matrix.txtimp_info.txt
Myd88 r is 1 
Found -/- in !Series_overall_design	"Bone marrow-derived macrophages from Myd88-/-Trif-/- and Myd88-/-Rip2-/- mice were infected with WT L. pneumophila (Lp02) or dotA mutant L. pneumophila (Lp03) for 4 hours. The RNA was extracted, processed, and hybridized onto Affymetrix 430 2.0 microarrays"
GSE13148_series_matrix.txtimp_info.txt
aggrecan r is 2 
Found induced in !Series_summary	"In the present microarray study, we set out to identify age- and arthritis-related gene expression pattern changes in proteoglycan (aggrecan)-induced arthritis (PGIA) model."
GSE13156_series_matrix.txtimp_info.txt
Crh r is 1 
Found treated in !Series_overall_design	"Two condition experiment: untreated vs. 100 nM Crh treated AtT-20 cells with a time curve of 1, 3, 6, 12, 24 hours. Technical replicates: 6 for each time point, including dye-swap each with 3 replicates"
GSE13160_series_matrix.txtimp_info.txt
Apo r is 4 
Found -/- in !Series_summary	"By means of Operon V3 microarrrays, the in vivo, aortic endothelial transcriptomic responses to chronic (30 day) whole body exposure to diesel exhaust were assessed in wild type and Apo E (-/-) mice.  The in vitro response of cultured Svec 4-10 cells exposed  to a soluble extract extract of diesel engine particulate were similarly assessed."
GSE13160_series_matrix.txtimp_info.txt
Apo r is 4 
Found -/- in !Series_overall_design	"Mice of the Tie 2 GFP strain as well as a stable hybrid strain derived by cross of Tie 2 GFP with the Apo E (-/-) strain were bred in suffficient quantities for these experiments.  Male mice at 4 months of age at the initiation of the exposure to 30 days of dilute diesel engine 94 hours/day, 5 days/week) at either 0 (control), 300 or 1000 ug/ cubic meter exhaust particulate.   Following exposure, three pooled aortae of each experimental and ceach c age-matched control group were dissected from the aortic arch to the iliac bifurcation, minced and collagenolytically digested prior to FACS into Trizol.  Purification yielded aortic endothelial RNA subjected to amplification with Nugen isothermal linear amplification to produce amplified cDNA.  Microarrays were performed with a single dye reversal to compare the transcriptome of exposed mice to age-matched control mice.  "
GSE13163_series_matrix.txtimp_info.txt
Deaf1 r is 1 
Found knock-out in !Series_summary	"A microarray study performed in the pancreatic lymph nodes of Deaf1 knock-out and BALB/c control mice to identify genes that are regulated by the transcriptional regulator Deaf1.  These experiments constitute a portion of the study described below:"
GSE13189_series_matrix.txtimp_info.txt
THP r is 3 
Found overexpressing in !Series_summary	"Expression of meningioma 1 (MN1) has been proposed to be a negative prognostic molecular marker in adult AML with normal cytogenetics, however its role in pediatric leukemia is unknown. We found elevated MN1 expression in 53 of 88 pediatric leukemia cases: significant amounts of MN1 were found in immature B-cell ALL and most cases of infant leukemia but no MN1 expression was detected in T-cell acute lymphoblastic leukemia (T-ALL). Interestingly 17 of 19 cases harboring MLL-X fusions showed also elevated MN1 expression. Lentiviral siRNA mediated MN1 knock-down resulted in cell cycle arrest and impaired clonogenic growth of 3 MLL-X-positive human leukemia cell lines overexpressing MN1 (THP-1, RS4;11, MOLM13). In a mouse MLL/ENL-induced leukemia MN1 overexpression resulted from retroviral provirus insertion. Strikingly co-expression of MN1 with MLL/ENL resulted in significantly reduced latency for induction of an AML phenotype in mice suggesting functional cooperation. MN1 overexpression in MLL/ENL-carrying cells resulted in expansion of the L-GMP population and facilitated disease induction in secondary recipients. Gene expression profiling allowed to define a number of potential MN1 hematopoietic targets. Up-regulation of CD34, FLT3, HLF, or DLK1 was validated in bone marrow transiently overexpressing MN1, in MN1-induced mouse leukemias, as well as in some cases of pediatric leukemias overexpressing MN1. Taken together, our work suggests that MN1 overexpression is essential for growth of leukemic cells, and that MN1 can act as a cooperating oncogene with MLL-X fusion genes most probably through modification of a distinct gene expression program that leads to expansion of a leukemia initiating cell population. "
GSE13190_series_matrix.txtimp_info.txt
Esrrb r is 5 
Found knockdown in !Series_title	"Global gene-expression analyses of the Esrrb reprogrammed cells and Esrrb knockdown cells"
GSE13190_series_matrix.txtimp_info.txt
Klf4 r is 7 
Found induced in !Series_summary	"In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming."
GSE13192_series_matrix.txtimp_info.txt
LXR r is 4 
Found treated in !Series_overall_design	"To study the importance of each of the receptor subtypes, myotube cultures derived from wild type (WT), LXRa and LXRb knockout (KO) mice were established. Sixteen samples were examined. Half the samples were treated with the unselective LXR agonist T0901317."
GSE13207_series_matrix.txtimp_info.txt
Sirt6 r is 1 
Found knockout in !Series_summary	"We completed genome-wide microarray analysis in Sirt6 knockout (ko) mouse embryonic fibroblasts (MEFs) and control wildtype (wt) MEFs. Prior to RNA extraction, MEFs were treated with TNF-alpha (10 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion Amino Allyl MessageAmp II Amplification kit. Amplified mouse Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008)."
GSE13207_series_matrix.txtimp_info.txt
Sirt6 r is 1 
Found -/- in !Series_title	"Mouse Sirt6-/- TNF-alpha timecourse"
GSE13207_series_matrix.txtimp_info.txt
TNF-alpha r is 2 
Found -/- in !Series_title	"Mouse Sirt6-/- TNF-alpha timecourse"
GSE13207_series_matrix.txtimp_info.txt
Sirt6 r is 3 
Found ko in !Series_summary	"We completed genome-wide microarray analysis in Sirt6 knockout (ko) mouse embryonic fibroblasts (MEFs) and control wildtype (wt) MEFs. Prior to RNA extraction, MEFs were treated with TNF-alpha (10 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion Amino Allyl MessageAmp II Amplification kit. Amplified mouse Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008)."
GSE13207_series_matrix.txtimp_info.txt
TNF-alpha r is 2 
Found treated in !Series_summary	"We completed genome-wide microarray analysis in Sirt6 knockout (ko) mouse embryonic fibroblasts (MEFs) and control wildtype (wt) MEFs. Prior to RNA extraction, MEFs were treated with TNF-alpha (10 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion Amino Allyl MessageAmp II Amplification kit. Amplified mouse Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008)."
GSE13208_series_matrix.txtimp_info.txt
Sirt6 r is 1 
Found -/- in !Series_title	"Mouse Sirt6-/- tissues"
GSE13208_series_matrix.txtimp_info.txt
Sirt6 r is 1 
Found -/- in !Series_summary	"We harvested liver, spleen, thymus, and skin tissues from 21 or 29 day old Sirt6-/- animals and then completed genome-wide microarray analysis. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Amino Allyl MessageAmp II Amplification kit. Amplified age-matched wild-type tissues were used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008)."
GSE13209_series_matrix.txtimp_info.txt
Sirt6 r is 1 
Found -/- in !Series_title	"Mouse Sirt6-/- RelA+/- tissues"
GSE13209_series_matrix.txtimp_info.txt
Sirt6 r is 1 
Found -/- in !Series_summary	"We harvested spleen tissue from Sirt6-/- or Sirt6-/- RelA+/- animals and then completed genome-wide microarray analysis. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Amino Allyl MessageAmp II Amplification kit. Amplified age-matched wild-type tissues were used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008)."
GSE13211_series_matrix.txtimp_info.txt
Klf4 r is 7 
Found induced in !Series_summary	"In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming."
GSE13212_series_matrix.txtimp_info.txt
Esrrb r is 2 
Found silencing in !Series_summary	"Global gene expression effects of silencing the Esrrb gene. We used microarrays to detail the global programme of gene expression after silencing the Esrrb gene."
GSE13212_series_matrix.txtimp_info.txt
Esrrb r is 1 
Found knockdown in !Series_title	"Global gene-expression analyses of the Esrrb knockdown cells"
GSE13212_series_matrix.txtimp_info.txt
Klf4 r is 7 
Found induced in !Series_summary	"In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming."
GSE13264_series_matrix.txtimp_info.txt
Sry r is 4 
Found treated in !Series_summary	"The purpose of this experiment was to determine the expression traits in Liver tissue from the Four Core Genotype treated group. Keywords: Sry transgene Four Core Genotype Mouse liver Tissue"
GSE13298_series_matrix.txtimp_info.txt
Rb1 r is 1 
Found deficient in !Series_overall_design	"We have compared 3 cecal tumors with 3 duodenal tumors from Rb1 deficient Apc1638N mice."
GSE13302_series_matrix.txtimp_info.txt
PPARalpha r is 2 
Found activation in !Series_summary	"Most of the transcriptional changes induced by PFOS in the fetal mouse liver and lung were related to activation of PPARalpha.  When compared to the transcript profiles induced by PFOA (Pubmed ID 17681415), few remarkable differences were found other than up-regulation of Cyp3a genes.  Because PFOS and PFOA have been shown to differ in their mode of action in the murine neonate, these data suggest that changes related to PFOS-induced neonatal toxicity may not be evident in the fetal transcriptome at term."
GSE13306_series_matrix.txtimp_info.txt
Foxp3 r is 8 
Found + in !Series_title	"Retinoic Acid Enhances Foxp3 Induction Indirectly by Relieving Inhibition from CD4(+)CD44(hi) Cells."
GSE13306_series_matrix.txtimp_info.txt
Foxp3 r is 1 
Found + in !Series_summary	"CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. This indirect effect was evident in vivo and required the expression of the RA receptor alpha. Thus, cytokine-producing CD44(hi) cells actively restrain TGF-beta-mediated Foxp3 expression in naive T cells, and this balance can be shifted or fine-tuned by RA."
GSE13312_series_matrix.txtimp_info.txt
p53 r is 5 
Found null in !Series_overall_design	"Gene expression patterns were compared between p53 wt MEF and p53-null MEF cells."
GSE13336_series_matrix.txtimp_info.txt
AngII r is 1 
Found overexpressing in !Series_title	"Gene expression profiling in cardiac AngII-overexpressing mice (TG1306/1R)"
GSE13364_series_matrix.txtimp_info.txt
BWF1 r is 8 
Found treated in !Series_summary	"Microarray analysis was performed on BWF1 mice spleenocyte cells in control and pCONS treated mice."
GSE13380_series_matrix.txtimp_info.txt
ovalbumin r is 3 
Found induced in !Series_overall_design	"The analysis includes 9 samples of genomic DNA from isolated splenic CD11c+ dendritic cells (>95% pure) per group. The two groups are neonates born to mothers with induced allergy to ovalbumin, and normal control neonates. All neonates are genetically and environmentally identical, and allergen-naive."
GSE13382_series_matrix.txtimp_info.txt
Foxa2 r is 5 
Found -/- in !Series_summary	"We analyzed the effects of these changes in FOXA transcription factor expression using Foxa2 transgenic mice and Foxa3-/- mice. We found that persistent expression of FOXA2 reduced mucus but the absence of FOXA3 had no effect on mucus production induced by allergen challenge."
GSE13382_series_matrix.txtimp_info.txt
Foxa3 r is 1 
Found -/- in !Series_summary	"We analyzed the effects of these changes in FOXA transcription factor expression using Foxa2 transgenic mice and Foxa3-/- mice. We found that persistent expression of FOXA2 reduced mucus but the absence of FOXA3 had no effect on mucus production induced by allergen challenge."
GSE13382_series_matrix.txtimp_info.txt
Foxa3 r is 1 
Found -/- in !Series_summary	"Keywords: gene expression comparison between Foxa3-/- and littermate control mice both challenged with OVA"
GSE13382_series_matrix.txtimp_info.txt
Foxa3 r is 1 
Found KO in !Series_overall_design	"DNA miocroarrays were used to analyze lung mRNA expression of Foxa3 KO and littermate control mice challenged with saline or OVA. The experiment incorporated a 1 color design and used Agilent arrays that contained roughly 44,000 60mer probes that provide complete coverage of the mouse genome. 11 arrays were hybridized and represent 3 lung samples for groups WT saline, WT OVA and KO OVA. There are 2 lung samples for the KO saline group."
GSE13402_series_matrix.txtimp_info.txt
SPARC r is 1 
Found null in !Series_summary	"SPARC is a matricellular glycoprotein involved in regulation of the extracellular matrix, growth factors, adhesion, and migration.  SPARC-null mice have altered basement membranes and develop posterior sub-capsular cataracts with cell swelling and equatorial vacuoles.  Exchange of fluid, nutrients, and waste products in the avascular lens is driven by a unique circulating ion current.  Here we demonstrate that SPARC-null mouse lenses exhibit abnormal circulation of fluid, ion, and small molecules which leads to altered fluorescein distribution in vivo, loss of resting membrane polarization, and altered distribution of small molecules.  Microarray analysis of SPARC-null lenses showed changes in gene expression of ion channels and receptors, matrix and adhesion genes, cytoskeleton, immune response genes, and cell signaling molecules.  Our results demonstrate that the regulation of SPARC on cell-capsular matrix interactions can influence the circulation of fluid and ions in the lens, and the phenotype in the SPARC-null mouse lens is the result of multiple intersecting pathways."
GSE13408_series_matrix.txtimp_info.txt
Rb r is 3 
Found knock-out in !Series_summary	"The retinoblastoma cell cycle regulator pRb and the two related proteins p107 and p130 are thought to suppress cancer development both by inhibiting the G1/S transition of the cell cycle in response to growth-arrest signals and by promoting cellular differentiation. Here, we investigated the phenotype of Rb family triple knock-out (TKO) embryonic stem cells as they differentiate in vivo and in culture. Confirming the central role of the Rb gene family in cell cycle progression, TKO mouse embryos did not survive past mid-gestation and differentiating TKO cells displayed increased proliferation and cell death. However, patterning and cell fate determination were largely unaffected in these TKO embryos. Furthermore, a number of TKO cells, including in the neural lineage, were able to exit the cell cycle in G1 and terminally differentiate. This ability of Rb family TKO cells to undergo cell cycle arrest was associated with the repression of target genes for the E2F6 transcription factor, uncovering a pRb-independent control of the G1/S transition of the cell cycle. These results show that the Rb gene family is required for proper embryonic development but is not absolutely essential to induce G1 arrest and differentiation in certain lineages."
GSE13416-GPL6096_series_matrix.txtimp_info.txt
Hnrpll r is 8 
Found silencing in !Series_summary	"Immunological Memory is characterized by a heightened recall response to a previously encountered antigen, resulting from clonal expansion of antigen-specific lymphocytes and differentiation into specialized memory cells. Differentiation of memory B cells involves irreversible encountered antigen, resulting from clonal expansion of antigen-specific lymphocytes and differentiation into specialised memory cells. Differentiation of memory B cells involves irrversible DNA rearrangements and mutations, but differentiation of memory T cells is less understood. In an ENU screen for mouse mutations affecting the proportion of T cells with known memory cell markers, such as the alternative spliced Ptprc isoform CD45RO, we identified an inducible RNA-binding protein of previously unknown function, hnRNPLL (gene symbol Hnrpll), whose mutation abolishes the regulated silencing of CD45RABC exons in T cells and other leukocytes. In the mutant, a single amino acid substitution destabilizes an RNA-recognition domain that binds with micromolar affinity to RNA containing the Ptprc ARS exon silencing sequence. Hnrpll mutations selectively diminishes T cell accumulation in peripheral lymphoid tissues but not proliferation. Exon array analysis of Hnrpll mutant naive and memory T cells reveals an extensive program of alternative mRNA splicing in memory T cells coordinated by hnRNPLL. A remarkable overlap with alternative splicing in neural tissues may reflect a co-opted strategy of RNA rearrangement for achieving immunological memory in T cells."
GSE13432_series_matrix.txtimp_info.txt
VEGFR2 r is 5 
Found activation in !Series_summary	"The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here we show that exposure of mice to cold led to conversion of white adipose tissue (WAT) to brown-like adipose tissue, accompanying the switch of an active angiogenic phenotype.  Gene expression profile analysis showed VEGF was upregulated via most likely hypoxia-independent PGC-1 transcriptional activation.  Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis, significantly impaired nonshivering thermogenesis capacity, and markedly reduced adipose metabolism.  Unexpectedly, VEGFR1 blockage resulted in opposite effects by increasing adipose vascularity and metabolism.  These findings demonstrate that VEGFR2 and VEGFR1 mediate polarized activities in modulating adipose angiogenesis and metabolism. Taken together, our findings have conceptual implications in applying angiogenesis modulators for the treatment of obesity and metabolic disorders."
GSE13432_series_matrix.txtimp_info.txt
PGC-1 r is 3 
Found activation in !Series_summary	"The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here we show that exposure of mice to cold led to conversion of white adipose tissue (WAT) to brown-like adipose tissue, accompanying the switch of an active angiogenic phenotype.  Gene expression profile analysis showed VEGF was upregulated via most likely hypoxia-independent PGC-1 transcriptional activation.  Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis, significantly impaired nonshivering thermogenesis capacity, and markedly reduced adipose metabolism.  Unexpectedly, VEGFR1 blockage resulted in opposite effects by increasing adipose vascularity and metabolism.  These findings demonstrate that VEGFR2 and VEGFR1 mediate polarized activities in modulating adipose angiogenesis and metabolism. Taken together, our findings have conceptual implications in applying angiogenesis modulators for the treatment of obesity and metabolic disorders."
GSE13432_series_matrix.txtimp_info.txt
VEGFR2 r is 5 
Found induced in !Series_summary	"The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here we show that exposure of mice to cold led to conversion of white adipose tissue (WAT) to brown-like adipose tissue, accompanying the switch of an active angiogenic phenotype.  Gene expression profile analysis showed VEGF was upregulated via most likely hypoxia-independent PGC-1 transcriptional activation.  Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis, significantly impaired nonshivering thermogenesis capacity, and markedly reduced adipose metabolism.  Unexpectedly, VEGFR1 blockage resulted in opposite effects by increasing adipose vascularity and metabolism.  These findings demonstrate that VEGFR2 and VEGFR1 mediate polarized activities in modulating adipose angiogenesis and metabolism. Taken together, our findings have conceptual implications in applying angiogenesis modulators for the treatment of obesity and metabolic disorders."
GSE13448_series_matrix.txtimp_info.txt
Mef r is 7 
Found -/- in !Series_overall_design	"RNAs isolated from wild type, p53 -/- and p53 -/- Mef -/-  LSK cells were used in oligonucleotide arrays (Affymetrix) "
GSE13448_series_matrix.txtimp_info.txt
p53 r is 2 
Found -/- in !Series_overall_design	"RNAs isolated from wild type, p53 -/- and p53 -/- Mef -/-  LSK cells were used in oligonucleotide arrays (Affymetrix) "
GSE13448_series_matrix.txtimp_info.txt
Gfi-1 r is 3 
Found null in !Series_summary	"The importance of the p53 protein in the cellular response to DNA damage is well known, but its function during steady-state hematopoiesis has not been established. We have defined a critical role of p53 in regulating hematopoietic stem cell quiescence, especially in promoting the enhanced quiescence seen in HSCs that lack the MEF/ELF4 transcription factor. Transcription profiling of HSCs isolated from wild type and p53 null mice identified Gfi-1 and Necdin as p53 target genes and using lentiviral vectors to upregulate or knockdown the expression of these genes, we show their importance in regulating HSC quiescence. Establishing the role of p53 (and its target genes) in controlling the cell cycle entry of HSCs may lead to therapeutic strategies capable of eliminating quiescent cancer (stem) cells."
GSE13467-GPL4128_series_matrix.txtimp_info.txt
Ezh1 r is 3 
Found overexpressing in !Series_overall_design	"Undifferentiated F9 cells were used for this experiment. Antibodies specificity were checked using a stable cell lines overexpressing a GAl4-Ezh1 or a Gal4-Ezh2 in an inducible manner followed by conventional ChIP at Gal4 responsive transgene. "
GSE13467-GPL4128_series_matrix.txtimp_info.txt
Ezh2 r is 7 
Found overexpressing in !Series_overall_design	"Undifferentiated F9 cells were used for this experiment. Antibodies specificity were checked using a stable cell lines overexpressing a GAl4-Ezh1 or a Gal4-Ezh2 in an inducible manner followed by conventional ChIP at Gal4 responsive transgene. "
GSE13467-GPL4129_series_matrix.txtimp_info.txt
Ezh1 r is 3 
Found overexpressing in !Series_overall_design	"Undifferentiated F9 cells were used for this experiment. Antibodies specificity were checked using a stable cell lines overexpressing a GAl4-Ezh1 or a Gal4-Ezh2 in an inducible manner followed by conventional ChIP at Gal4 responsive transgene. "
GSE13467-GPL4129_series_matrix.txtimp_info.txt
Ezh2 r is 7 
Found overexpressing in !Series_overall_design	"Undifferentiated F9 cells were used for this experiment. Antibodies specificity were checked using a stable cell lines overexpressing a GAl4-Ezh1 or a Gal4-Ezh2 in an inducible manner followed by conventional ChIP at Gal4 responsive transgene. "
GSE13490_series_matrix.txtimp_info.txt
p53 r is 1 
Found -/- in !Series_overall_design	"This study features two factors, injected cell origin (either tumorsphere or neurosphere) and FACS cell population (either side population or non-side population cells).  There were two different tumorspheres, labeled 3447 and 4346 that were isolated from brain tumors in S100beta-verbB;p53-/- or S100beta-verbB;p53+/- mice.  The tumorspheres were injected separately into the brains of NOD.Cg-Prkdc<scid>Il2rg<tm1Wjl>/SzJ mice to generate biological triplicates of each primary tumor.  Tumorspheres were isolated and cultured before FACS sorting to obtain side population and non-side population cells.  As a control, untransformed neurospheres from three independent S100beta-verbB;p53-/- or S100beta-verbB;p53+/- mice were isolated, cultured, and FACS sorted to obtain side population and non-side population cells.  Side population and non-side population cells cultured from three mice injected with the 3447 cultured tumorspheres were assayed for gene expression (six samples).  Side-population stem cells cultured from three mice injected with the 4346 cultured tumorspheres were assayed for gene expression (three samples).  Side-population and non-side population cells cultured from three mice injected with the neurospheres were assayed for gene expression (six samples).   "
GSE13493_series_matrix.txtimp_info.txt
Rag2 r is 1 
Found deficient in !Series_title	"Expression data from developing thymocytes of N15TCR transgenic Rag2 deficient mice"
GSE13493_series_matrix.txtimp_info.txt
TCR r is 3 
Found deficient in !Series_summary	"We used microarrays to identify the genes differentially expressed during CD8 single positive T cell development in N15 TCR transgenic Rag2 deficient mice."
GSE13493_series_matrix.txtimp_info.txt
Rag2 r is 1 
Found deficient in !Series_summary	"We used microarrays to identify the genes differentially expressed during CD8 single positive T cell development in N15 TCR transgenic Rag2 deficient mice."
GSE13493_series_matrix.txtimp_info.txt
TCR r is 4 
Found -/- in !Series_overall_design	"We have analyzed gene expression in the individual populations as development proceeds from DP, intermediate (Int), to SP subsets. To this end, we sorted the individual populations from six age and sex matched 5-6 week old N15 TCR tg+/+ RAG-2-/- H-2b mice for two independent experiments. For sorting subpopulations, cells were stained with anti-CD4 (L3T4) and anti-CD8 (Ly-2) antibodies (Pharmingen, San Diego, CA USA) and DP, Int and SP thymocytes were sorted on a MoFlo (Cytomation, Fort Collins, CO USA)."
GSE13522_series_matrix.txtimp_info.txt
IFN-gamma r is 2 
Found deficient in !Series_summary	"We used microarrays to detail the local host transcriptional response to intradermal T. cruzi infection in WT mice and mice depleted of NK cells, or deficient in IFN-gamma or type I IFN responses. Additionally we compared the local host-transcriptional response generated to infection with 3 different strains of Trypanosoma cruzi (Y, Brazil, and G)."
GSE13522_series_matrix.txtimp_info.txt
IFN-gamma r is 2 
Found KO in !Series_overall_design	"Mice were infected by intradermal injection of 10^6 T. cruzi trypomastigotes in 100uL of saline split between 2 adjacent sites on the shaved side flank.  Control mice were injected with an equal volume of saline. 24 hours post-injection approximately 75mm^2 of skin immediately surrounding the injection site was excised and RNA was isolated from the tissue. Balb/c mice were used for most experiments and IFN-gamma KO mice were on the Balb/c background. WT 129 mice were also used as IFNAR-/- mice were on the 129 background. In total 33 arrays were performed. 7 WT (Balb/c) control, 3 Y strain infected, 3 Brazil strain infected, 3 G strain infected, 2 IFN-gamma KO control, 2 IFN-gamma KO infected, 1 NK cell depleted control, 1 NK cell depleted infected, 3 WT (129) control, 3 WT (129) infected, 3 IFNAR KO control, 3 IFNAR KO infected"
GSE13526_series_matrix.txtimp_info.txt
Nxf2 r is 1 
Found KO in !Series_title	"Transcript profiling of WT and Nxf2 KO post-natal day 21 testes"
GSE13526_series_matrix.txtimp_info.txt
Nxf2 r is 3 
Found KO in !Series_summary	"We used microarrays to check the expression profiles of the Nxf2 WT and KO 21d testes on C57BL/6 background."
GSE13526_series_matrix.txtimp_info.txt
Nxf2 r is 1 
Found KO in !Series_overall_design	"To examine the expression difference between WT and Nxf2 KO testes, we collected testes from juvenile mice of three ages ( 21d, 26d, 28d). Testis weight was similar between WT and KO mice at post-natal day 21.  Three pairs of WT and KO 21d testes were chosen for microarray analysis."
GSE13526_series_matrix.txtimp_info.txt
Nxf2 r is 1 
Found mutant in !Series_summary	"In euakryotes, mRNAs must be exported from the nucleus to the cytsoplasm. NXF2 is highly expressed in the mouse male germ cells.  We are interested in its function in spermatogenesis, espically in the nuclear RNA export in the testis. To this end, we made Nxf2 mutant mice by gene targeting. In an attempt to identify the mRNA substrates of NXF2, we perform the microarray experiments on testes."
GSE13579_series_matrix.txtimp_info.txt
Bmal1 r is 1 
Found mutant in !Series_summary	"Hair follicles undergo recurrent cycling of controlled growth (anagen), regression (catagen), and relative quiescence (telogen) with a defined periodicity. Taking a genomics approach to study gene expression during synchronized mouse hair follicle cycling, we discovered that, in addition to circadian fluctuation, CLOCK-regulated genes are also modulated in phase with the hair growth cycle. During telogen and early anagen, circadian clock genes are prominently expressed in the secondary hair germ, which contains precursor cells for the growing follicle. Analysis of Clock and Bmal1 mutant mice reveals a delay in anagen progression, and the secondary hair germ cells show decreased levels of phosphorylated Rb and lack mitotic cells, suggesting that circadian clock genes regulate anagen progression via their effect on the cell cycle. Consistent with a block at the G1 phase of the cell cycle, we show a significant upregulation of p21 in Bmal1 mutant skin. While circadian clock mechanisms have been implicated in a variety of diurnal biological processes, our findings indicate that circadian clock genes may be utilized to modulate the progression of non-diurnal cyclic processes."
GSE13582_series_matrix.txtimp_info.txt
KRAP r is 1 
Found deficient in !Series_title	"Expression data from BAT of the KRAP deficient mice"
GSE13582_series_matrix.txtimp_info.txt
KRAP r is 1 
Found deficient in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13582_series_matrix.txtimp_info.txt
KRAP r is 4 
Found -/- in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13582_series_matrix.txtimp_info.txt
Ki r is 2 
Found induced in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13582_series_matrix.txtimp_info.txt
ras r is 1 
Found induced in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13583_series_matrix.txtimp_info.txt
KRAP r is 1 
Found deficient in !Series_title	"Expression data from liver of the KRAP deficient mice "
GSE13583_series_matrix.txtimp_info.txt
KRAP r is 1 
Found deficient in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. "
GSE13583_series_matrix.txtimp_info.txt
KRAP r is 4 
Found -/- in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. "
GSE13583_series_matrix.txtimp_info.txt
Ki r is 2 
Found induced in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. "
GSE13583_series_matrix.txtimp_info.txt
ras r is 1 
Found induced in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. "
GSE13585_series_matrix.txtimp_info.txt
KRAP r is 1 
Found deficient in !Series_title	"Expression data from BAT and liver of the KRAP deficient mice"
GSE13585_series_matrix.txtimp_info.txt
KRAP r is 1 
Found deficient in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13585_series_matrix.txtimp_info.txt
KRAP r is 4 
Found -/- in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13585_series_matrix.txtimp_info.txt
Ki r is 2 
Found induced in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13585_series_matrix.txtimp_info.txt
ras r is 1 
Found induced in !Series_summary	"KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule.  KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia.  KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia."
GSE13588_series_matrix.txtimp_info.txt
Foxp2 r is 4 
Found ko in !Series_title	"Gene expression in striatums of Foxp2-hum, Foxp2-ko and wild-type mice"
GSE13592_series_matrix.txtimp_info.txt
Apoe r is 2 
Found deficient in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13592_series_matrix.txtimp_info.txt
apolipoprotein E r is 2 
Found deficient in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13592_series_matrix.txtimp_info.txt
Apoe r is 1 
Found -/- in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13592_series_matrix.txtimp_info.txt
apolipoprotein E r is 5 
Found -/- in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13592_series_matrix.txtimp_info.txt
Ccl17 r is 1 
Found expressing in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13599_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found knockout in !Series_summary	"This study aims on the identification of the NF-kB dependent gene regulatory network during inflammation-associated liver carcinogenesis using the well-established Mdr2 knockout mouse model. We could identify 367 differentially expressed genes comparing expression profiles of tumor samples from Mdr2-KO mice to tumor samples derived from mice with an additional hepatocyte specific expression of an IkB-superrepressor. This IkB-superrepresser is undegradable upon ubiquitinylation initialized by Ikk dependent phosphorylation and therefore impedes NFkB activity."
GSE13599_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found knockout in !Series_overall_design	"In the experiments shown here, we compare gene expression profiles of HCCs from 4 idividual mice harboring a biallelic Mdr2 knockout to HCC specimen of 6 individual mice with Mdr2 knockout and a hepatocyte specific expression of the IkB-superrepressor. Each individual sample was hybridized aginst a universal reference mouse pool (Stratagene) on a two-color microarray. Furthermore was each sample/reference hybridization conducted as a dye swap experiment yielding two technical replicates with inverted dye channel orientation per sample. In addition a biological control using wildtype liver tissue from mice of the same genetic background was hybridized the same way aginst a universal reference. The latter was used to build a sample/control ratio for displays of indirect comparison."
GSE13599_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found KO in !Series_title	"NFkB dependent gene expression in a Mdr2-KO hepatocellular carcinoma (HCC) mouse model using a IkB-Superrepressor"
GSE13599_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found KO in !Series_summary	"Keywords: NFkB, IkB-superrepressor, inflammation-associated liver carcinogenesis, Mdr2-KO mouse model, hepatocellular carcinoma, gene expression, microarray"
GSE13626_series_matrix.txtimp_info.txt
VAP-1 r is 3 
Found -/- in !Series_title	"Comparison of gene expression in melanoma of wild-type and VAP-1 -/- mice"
GSE13626_series_matrix.txtimp_info.txt
VAP-1 r is 3 
Found -/- in !Series_overall_design	"The B16-F10-Luc-G5 melanoma cells (Xenogen) were injected subcutaneously into abdominal area of 2 wild-type and 2 VAP-1 -/- mice. Tumors were grown until day 10 when mice were euthanized. Tumors were dissected and total RNA was isolated using the Qiagen RNA extraction kit."
GSE13635_series_matrix.txtimp_info.txt
cyclin r is 3 
Found -/- in !Series_title	"Gene expression change in cyclin D1 -/- retinas in comparison to wildtype."
GSE13635_series_matrix.txtimp_info.txt
cyclin D1 r is 3 
Found -/- in !Series_title	"Gene expression change in cyclin D1 -/- retinas in comparison to wildtype."
GSE13635_series_matrix.txtimp_info.txt
D1 r is 2 
Found -/- in !Series_title	"Gene expression change in cyclin D1 -/- retinas in comparison to wildtype."
GSE13642_series_matrix.txtimp_info.txt
Apoe r is 2 
Found deficient in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13642_series_matrix.txtimp_info.txt
apolipoprotein E r is 2 
Found deficient in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13642_series_matrix.txtimp_info.txt
Apoe r is 1 
Found -/- in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13642_series_matrix.txtimp_info.txt
apolipoprotein E r is 5 
Found -/- in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13642_series_matrix.txtimp_info.txt
Ccl17 r is 1 
Found expressing in !Series_summary	"Dendritic cells (DCs) are essential for priming of immune responses. Although immune mechanisms are known to control the pathogenesis of atherosclerosis, the role of DCs remains elusive. Here we show that Ccl17 expressing mature, myeloid DCs accumulate within atherosclerotic lesions. Deletion of Ccl17 in apolipoprotein E-deficient (Apoe-/-) mice reduces the development and progression of atherosclerosis in several disease models. While Ccl17 expression by DCs dampened antigen-specific T cell proliferation, it is required for efficient polarization of T helper type 1 (Th1) and Th17 as reflected by a preponderance of Th2 cytokines in Ccl17-/- Apoe-/- mice. In line with these findings, only transfer of T cells from Apoe-/-, but not from Ccl17-/- Apoe-/- precipitated atherosclerosis in T cell depleted Apoe-/- recipients. These findings identify Ccl17+ DCs as central immune regulators in atherosclerosis and Ccl17 as a potential target in the treatment of this disease."
GSE13643_series_matrix.txtimp_info.txt
ALS r is 4 
Found mutant in !Series_summary	"To better understand how the expression of a mutant gene that causes ALS can perturb the normal phenotype of astrocytes, and to identify genes that may have a role in their toxic effect on motor neurons, we used oligonucleotide arrays to compare the global gene expression profiles of glia overexpressing the mutant SOD1G93A protein with two different sets of controls: non-transgenic glia and glia overexpressing the wild type form of the human SOD1 protein (P<0.001) ."
GSE13645_series_matrix.txtimp_info.txt
p56Lck r is 6 
Found null in !Series_summary	"Signaling through the T cell antigen receptor is essential for the formation of regulatory T (Treg) cells in the thymus and for their involvement in antigen-directed suppression of immune responses.  Using a conditional null allele of the gene encoding p56Lck we show here that T cell antigen receptor (TCR) signaling is also essential for sustaining the phenotype and homeostasis of Treg cells.  Inactivation of p56Lck in Treg cells resulted in large-scale changes in their gene expression profile, blocked their capacity to suppress responses, inhibited their proliferation, and caused them to redistribute in the body.  The results make clear multiple aspects of the Treg cell phenotype that are dependent on a sustained capacity to respond through their TCRs."
GSE13665_series_matrix.txtimp_info.txt
Crhr1 r is 4 
Found knockout in !Series_title	"Pituitaries of basal and stressed Crhr1 wild type and knockout mice"
GSE13665_series_matrix.txtimp_info.txt
Crhr1 r is 7 
Found knockout in !Series_summary	"Pituitaries of basal and stressed Crhr1-wildtype (wt) and -knockout (ko) mice (Timpl et al., 1998)"
GSE13685_series_matrix.txtimp_info.txt
kappa r is 3 
Found activation in !Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappa-B, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."
GSE13685_series_matrix.txtimp_info.txt
NF r is 2 
Found activation in !Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappa-B, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."
GSE13686_series_matrix.txtimp_info.txt
Mef2c r is 1 
Found deficient in !Series_overall_design	"Expression profiles of multipotent progenitor cells (MPPs) from Mef2c deficient (Mx1-Cre Mef2cf/f  ) mice where compared to MPPs from control (Mef2cf/f  ) mice in triplicate."
GSE13686_series_matrix.txtimp_info.txt
Mx1 r is 2 
Found deficient in !Series_overall_design	"Expression profiles of multipotent progenitor cells (MPPs) from Mef2c deficient (Mx1-Cre Mef2cf/f  ) mice where compared to MPPs from control (Mef2cf/f  ) mice in triplicate."
GSE13688_series_matrix.txtimp_info.txt
constitutive androstane receptor r is 6 
Found activation in !Series_summary	"TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene) and PCN (pregnenolone 16α-carbonitrile) are inducers of drug metabolism through activation of nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor), respectively. Mouse experiment was designed to study the effect of CAR and PXR activation on cholesterol homeostasis genes and other genes, which are present on the Steroltalk v2 microarray. Treatments were combined with standard and high-cholesterol diet to observe the interference of high liver cholesterol on nuclear receptor transcription regulation. All experiments were done within the European sixth Framework program “Steroltalk” (www.steroltalk.net). Results form these experiments give new knowledge about involvement of ‘xenosensors’ CAR and PXR in regulation of endogenous liver metabolism."
GSE13707_series_matrix.txtimp_info.txt
myostatin r is 2 
Found knockout in !Series_summary	"More than 2,000 genes appear to be upregulated or downregulated in skeletal muscle of mice with constitutive knockout of myostatin (Steelman et al., FASEB J 20:580-2, 2006). This study was done to determine whether inhibition of myostatin activity in mature mice has similar effects on the pattern of gene expression."
GSE13718_series_matrix.txtimp_info.txt
trap r is 5 
Found deficient in !Series_summary	"Background: The ErbB3 binding protein-1 (Ebp1) belongs to a family of DNA/RNA binding proteins implicated in cell growth, apoptosis and differentiation. However, the physiological role of Ebp1 in the whole organism is not known. Therefore, we generated Ebp1-deficient mice carrying a gene trap insertion in intron 2 of  the Ebp1 (pa2g4) gene."
GSE13718_series_matrix.txtimp_info.txt
Ebp1 r is 2 
Found -/- in !Series_summary	"Results: Ebp1 -/- mice were on average 30% smaller than wild type and heterozygous sex matched littermates. Growth retardation was apparent from Day 10 until Day 30. IGF-1 production and IGBP-3 and 4 protein levels were reduced in  both embryo fibroblasts and adult knock-out mice. The proliferation of fibroblasts derived from Day 12.5  knock out embryos was also decreased as compared to that of wild type cells. Microarray expression analysis revealed changes in genes important in cell growth including members of the MAPK signal transduction pathway. In addition, the expression or activation of proliferation related genes such as AKT and the androgen receptor, previously demonstrated to be affected by Ebp1 expression in vitro,  were altered in adult tissues."
GSE13719_series_matrix.txtimp_info.txt
aryl hydrocarbon receptor r is 3 
Found activation in !Series_summary	"Effect of the over activation of the aryl hydrocarbon receptor on gene expression of spleen derived dendritic cells. "
GSE13730_series_matrix.txtimp_info.txt
aggrecan r is 1 
Found induced in !Series_summary	"BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), a murine model of rheumatoid arthritis (Glant,T.T. and Mikecz,K., Proteoglycan aggrecan-induced arthritis.  A murine autoimmune model of rheumatoid arthritis. Methods Mol.Med. 2004. 102: 313-338.). However, there are marked differences among BALB/c colonies (maintained by different vendors at different locations) in PGIA onset and severity, which could be the result of subtle variations in their genetic background."
GSE13730_series_matrix.txtimp_info.txt
PG r is 3 
Found induced in !Series_summary	"BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), a murine model of rheumatoid arthritis (Glant,T.T. and Mikecz,K., Proteoglycan aggrecan-induced arthritis.  A murine autoimmune model of rheumatoid arthritis. Methods Mol.Med. 2004. 102: 313-338.). However, there are marked differences among BALB/c colonies (maintained by different vendors at different locations) in PGIA onset and severity, which could be the result of subtle variations in their genetic background."
GSE13740_series_matrix.txtimp_info.txt
NF r is 2 
Found activation in !Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappaB, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."
GSE13740_series_matrix.txtimp_info.txt
NF-kappaB r is 2 
Found activation in !Series_summary	"Pneumonia is a serious problem worldwide.  We recently demonstrated that innate defense mechanisms of the lung are highly inducible against pneumococcal pneumonia.  To determine the breadth of protection conferred by stimulation of lung mucosal innate immunity, and to identify cells and signaling pathways activated by this treatment, mice were treated with an aerosolized bacterial lysate, then challenged with lethal doses of bacterial and fungal pathogens.  Mice were highly protected against a broad array of Gram-positive, Gram-negative, and Class A bioterror bacterial pathogens, and Aspergillus fumigatus.  Protection was associated with rapid pathogen killing within the lungs, and this effect was recapitulated in vitro using a respiratory epithelial cell line.  Gene expression analysis of lung tissue showed marked activation of NF-kappaB, Type I and II interferon, and antifungal Card9-Bcl10-Malt1 pathways.  Cytokines were the most strongly induced genes, but the inflammatory cytokines TNF and IL-6 were not required for protection.  Lung-expressed antimicrobial peptides were also highly upregulated.  Taken together, stimulated innate resistance (StIR) appears to occur through the activation of multiple host defense signaling pathways in lung epithelial cells, inducing rapid pathogen killing, and conferring broad protection against virulent bacterial and fungal pathogens.  Augmentation of innate antimicrobial defenses of the lungs might have therapeutic value for protection of patients with neutropenia or impaired adaptive immunity against opportunistic pneumonia, and for defense of immunocompetent subjects against a bioterror threat or epidemic respiratory infection."
GSE13753_series_matrix.txtimp_info.txt
Rb r is 4 
Found knock-out in !Series_overall_design	"In one experiment, embryonic Day 13.5 placentas from wild-type and Rb -/- knock-out mice were compared. In the second experiment, embronic day 11.5 placentas from wild-type and Rb -/-;E2f4 -/- double knock-out mice were compared."
GSE13753_series_matrix.txtimp_info.txt
E2f4 r is 6 
Found -/- in !Series_summary	"Homozygous mutation of the murine retinoblastoma tumor suppressor gene, Rb, results in embryonic lethality between E13.5 and E15.5 with defects in cellular proliferation, differentiation and apoptosis.  Many of these defects are suppressed by mutation of an activating E2F, E2f1 or E2f3, indicating that they are key downstream targets of the retinoblastoma protein, pRB. In this study, we assess how E2F4 contributes to the developmental consequences of pRb-loss.  In stark contrast to the activating E2Fs, the homozygous mutation of E2f4 shortened the lifespan of Rb-/- embryos. This resulted from an exacerbation of the placental defect of the Rb-/- mice indicating that E2F4 and pRB cooperate in the development of this tissue. Further analyses indicated that this defect reflects an increase in trophectoderm-like cells. Under conditions where the placenta was wild-type but the embryo mutant for E2f4 and pRb embryos survived to birth and exhibited all of the defects that were observed in the E2f4 and Rb single mutant embryos. Thus, while pRB and E2F4 cooperate in placental development, they play largely non-overlapping roles the development of many embryonic tissues."
GSE13753_series_matrix.txtimp_info.txt
Rb r is 2 
Found -/- in !Series_overall_design	"In one experiment, embryonic Day 13.5 placentas from wild-type and Rb -/- knock-out mice were compared. In the second experiment, embronic day 11.5 placentas from wild-type and Rb -/-;E2f4 -/- double knock-out mice were compared."
GSE13772_series_matrix.txtimp_info.txt
apoA-I r is 2 
Found treated in !Series_overall_design	"Three replicate experiments were analyzed.  Each experiment consisted of a control sample and an apoA-I treated sample of RNA extracted from peritoneal macrophages isolated from both MyD88 +/+ and MyD88-/- mice, totaling four samples per experiment; 12 samples together."
GSE13772_series_matrix.txtimp_info.txt
apoA-I r is 2 
Found induced in !Series_title	"The apoA-I induced transcriptome and dependence on MyD88"
GSE13805_series_matrix.txtimp_info.txt
calreticulin r is 1 
Found deficient in !Series_title	"Expression data from wild type and calreticulin deficient murine embryonic stem cells"
GSE13805_series_matrix.txtimp_info.txt
calreticulin r is 1 
Found knockout in !Series_overall_design	"Stem cells cultured in triplicate (or more) were pooled to provide raw material per sample. Each sample represents  material collected from three technical replicates or more. In this manner, two wild type samples, and five derived from calreticulin knockout samples, were obtained. Although sample content contains material from three or more technical replicates harvested contemporaneously, each sample is a distinct biological replicate.  Total RNA was extracted from each of the samples and RNA pools were profiled on Affymetrix Mouse 430 2.0 Arrays to identify global gene expression changes invoked by genomic ablation of calreticulin."
GSE13835_series_matrix.txtimp_info.txt
apolipoprotein E r is 2 
Found deficient in !Series_summary	"This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant regions of the aorta of C57Bl/6 mice. In a parallel experiment, both regions were compared in young, plaque-free apolipoprotein E-deficient (apoE-/-) mice. Aortas of 3 male and 3 female C57Bl6 mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and an atherosclerosis-resistant region (TA: central thoracic aorta,i.e. 6 mm distal from the proximal 2mm of the thoracic aorta). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 70 genes. Up- or downregulation in the AA was observed for 33 and 37 genes respectively. Differential expression of 3 genes (ATPase, Na+/K+ transporting, beta 1 polypeptide, sarcolipin and homeo box B7) was confirmed using real-time PCR. Twenty five genes showed exclusively differential expression in C57BL6 mice. Only 7 could be linked to specific processes: development (4) and cell growth (3). The other 18 genes were all involved in different processes. Among the 45 genes showing differential expression in C57Bl/6 as well as apoE-/- mice, most were related to development (13), cell growth (8) and transcription (10). These results point to an altered transcriptome in SMCs of the C57Bl/6 aorta at an atherosclerosis-prone location. This is in agreement with findings in endothelial cells in atherosclerosis-prone regions. It could be due to biomechanical differences, for instance in wall tension or shear stress, or the different embryological origin of SMCs in AA and TA."
GSE13835_series_matrix.txtimp_info.txt
apolipoprotein E r is 5 
Found -/- in !Series_summary	"This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant regions of the aorta of C57Bl/6 mice. In a parallel experiment, both regions were compared in young, plaque-free apolipoprotein E-deficient (apoE-/-) mice. Aortas of 3 male and 3 female C57Bl6 mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and an atherosclerosis-resistant region (TA: central thoracic aorta,i.e. 6 mm distal from the proximal 2mm of the thoracic aorta). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 70 genes. Up- or downregulation in the AA was observed for 33 and 37 genes respectively. Differential expression of 3 genes (ATPase, Na+/K+ transporting, beta 1 polypeptide, sarcolipin and homeo box B7) was confirmed using real-time PCR. Twenty five genes showed exclusively differential expression in C57BL6 mice. Only 7 could be linked to specific processes: development (4) and cell growth (3). The other 18 genes were all involved in different processes. Among the 45 genes showing differential expression in C57Bl/6 as well as apoE-/- mice, most were related to development (13), cell growth (8) and transcription (10). These results point to an altered transcriptome in SMCs of the C57Bl/6 aorta at an atherosclerosis-prone location. This is in agreement with findings in endothelial cells in atherosclerosis-prone regions. It could be due to biomechanical differences, for instance in wall tension or shear stress, or the different embryological origin of SMCs in AA and TA."
GSE13836_series_matrix.txtimp_info.txt
apolipoprotein E r is 2 
Found deficient in !Series_summary	"This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant aorta segments in 4 months old apolipoprotein E-deficient (apoE-/-) mice before plaque development. In a parallel experiment, both regions were compared in young C57Bl/6 mice. Aortas of 3 male and 3 female ApoE-/- mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and a resistant region (TA: central thoracic aorta, i.e. 6 mm distal from the proximal 2 mm). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 244 genes. Up- or downregulation in the AA was observed for 186 and 58 genes respectively. Differential expression of 6 genes was confirmed using real-time PCR. The 201 genes that showed exclusively differential expression in apoE-/- mice were related to processes involved in atherosclerosis, such as cell adhesion, proliferation, differentiation, motility and death, lipid metabolism and immune responses. Furthermore, the transcription profile of the AA was in accordance with a more synthetic SMC phenotype. These results point to an altered transcriptome in SMCs in the aorta of apoE-/- mice at the atherosclerosis-prone location before actual lesion development. This suggests that SMCs, in addition to endothelial cells, can facilitate plaque formation at predilection sites."
GSE13836_series_matrix.txtimp_info.txt
apolipoprotein E r is 5 
Found -/- in !Series_summary	"This study compared gene expression in smooth muscle cells (SMCs) in atherosclerosis-prone and atherosclerosis-resistant aorta segments in 4 months old apolipoprotein E-deficient (apoE-/-) mice before plaque development. In a parallel experiment, both regions were compared in young C57Bl/6 mice. Aortas of 3 male and 3 female ApoE-/- mice were isolated, perfused with triton X-100 to remove endothelial cells and divided in an atherosclerosis-prone region (AA: ascending aorta, aortic arch and proximal 2 mm of thoracic aorta) and a resistant region (TA: central thoracic aorta, i.e. 6 mm distal from the proximal 2 mm). Microarray analysis (VIB-MAF) of pooled total RNA showed differential expression (>2-fold difference) for 244 genes. Up- or downregulation in the AA was observed for 186 and 58 genes respectively. Differential expression of 6 genes was confirmed using real-time PCR. The 201 genes that showed exclusively differential expression in apoE-/- mice were related to processes involved in atherosclerosis, such as cell adhesion, proliferation, differentiation, motility and death, lipid metabolism and immune responses. Furthermore, the transcription profile of the AA was in accordance with a more synthetic SMC phenotype. These results point to an altered transcriptome in SMCs in the aorta of apoE-/- mice at the atherosclerosis-prone location before actual lesion development. This suggests that SMCs, in addition to endothelial cells, can facilitate plaque formation at predilection sites."
GSE13855-GPL7726_series_matrix.txtimp_info.txt
p75 r is 6 
Found KO in !Series_title	"p55 and p75 tumor necrosis factor receptor double KO and systemic lupus erythematosis"
GSE13855-GPL7726_series_matrix.txtimp_info.txt
tumor necrosis factor r is 5 
Found KO in !Series_title	"p55 and p75 tumor necrosis factor receptor double KO and systemic lupus erythematosis"
GSE13855-GPL7747_series_matrix.txtimp_info.txt
p75 r is 6 
Found KO in !Series_title	"p55 and p75 tumor necrosis factor receptor double KO and systemic lupus erythematosis"
GSE13855-GPL7747_series_matrix.txtimp_info.txt
tumor necrosis factor r is 5 
Found KO in !Series_title	"p55 and p75 tumor necrosis factor receptor double KO and systemic lupus erythematosis"
GSE13859_series_matrix.txtimp_info.txt
estrogen receptor r is 3 
Found knockout in !Series_title	"Global survey of miRNA microarray of whole embryo, wild type vs estrogen receptor alpha knockout mice"
GSE13869_series_matrix.txtimp_info.txt
Nxnl1 r is 1 
Found -/- in !Series_title	"Transcriptome of the Nxnl1-/- mouse retina"
GSE13873_series_matrix.txtimp_info.txt
Rag-1 r is 7 
Found deletion in !Series_overall_design	"We chose mice for gene expression profiling that following Helicobacter infection had (a) symptoms of gastritis, but no epithelial changes, (b) atrophic gastritis accompanied by corpus gland hyperplasia or (c) atrophic gastritis accompanied by intestinal metaplasia. An uninfected control group was also included in the analysis, as were two groups of mice that lacked mature T- and B-cells due to a deletion mutation in the rag1 gene (Rag-1-/-) and that were either experimentally infected or served as Rag-1-/- uninfected controls. To see the effects of IFNg on murine gastric epithelial cells we analysed an immortalized murine primary gastric epithelial cell line treated with three different concentrations of IFNg in comparison to an untreated control."
GSE13873_series_matrix.txtimp_info.txt
Rag-1 r is 2 
Found -/- in !Series_overall_design	"We chose mice for gene expression profiling that following Helicobacter infection had (a) symptoms of gastritis, but no epithelial changes, (b) atrophic gastritis accompanied by corpus gland hyperplasia or (c) atrophic gastritis accompanied by intestinal metaplasia. An uninfected control group was also included in the analysis, as were two groups of mice that lacked mature T- and B-cells due to a deletion mutation in the rag1 gene (Rag-1-/-) and that were either experimentally infected or served as Rag-1-/- uninfected controls. To see the effects of IFNg on murine gastric epithelial cells we analysed an immortalized murine primary gastric epithelial cell line treated with three different concentrations of IFNg in comparison to an untreated control."
GSE13935_series_matrix.txtimp_info.txt
Bapx1 r is 4 
Found deficient in !Series_title	"Gene expression in pylorus stomach tissue in Bapx1 (Nkx3.2) deficient mice"
GSE13935_series_matrix.txtimp_info.txt
Bapx1 r is 1 
Found deficient in !Series_summary	"Bapx1 (Nkx3.2) is an important factor for GI development.  We document a morphologic change in the pylorus segment of the GI tract in Bapx1 deficient mice and we have used microarray analyses to assess gene exprofiles in the pylorus stomach region in knockout compared to wildtype littermates."
GSE13935_series_matrix.txtimp_info.txt
Bapx1 r is 2 
Found deficient in !Series_summary	"Keywords: Genetic modiufied mice deficient in Bapx1 expression"
GSE13935_series_matrix.txtimp_info.txt
Bapx1 r is 1 
Found knockout in !Series_overall_design	"RNA from 3 Bapx1 knockout animals and 3 control wildtype littermates were analyzed."
GSE13974_series_matrix.txtimp_info.txt
serine racemase r is 2 
Found inactivation in !Series_title	"Genetic inactivation of serine racemase produces behavioral phenotypes related to schizophrenia in mice"
GSE13979_series_matrix.txtimp_info.txt
bFGF r is 1 
Found treated in !Series_overall_design	"To determine whether there were shared transcriptional effects between reversible and irreversible AIG, we performed global microarray analyses on colonies isolated from soft agar for both bFGF-treated JB6 cells and fully tumorigenic JB6 cells from the RT101 cell line.  Gene expression changes associated with colony formation were determined by comparison to respective monolayer control cells."
GSE13981_series_matrix.txtimp_info.txt
Ccna2 r is 2 
Found knockdown in !Series_title	"Global gene expression profiles in Oct4-knockdown and Ccna2-knockdown mouse embryos."
GSE13981_series_matrix.txtimp_info.txt
Oct4 r is 1 
Found knockdown in !Series_title	"Global gene expression profiles in Oct4-knockdown and Ccna2-knockdown mouse embryos."
GSE13981_series_matrix.txtimp_info.txt
Ccna2 r is 1 
Found knockdown in !Series_summary	"Distinct subsets of genes are differentially expressed between Oct4 and Ccna2-knockdown embryos, and indicated differential functions.  Further, a large panel of genes were confirmed to be differentially-expressed in Oct4-knockdown embryos by quantitative, real time RT-PCR."
GSE13981_series_matrix.txtimp_info.txt
Oct4 r is 3 
Found knockdown in !Series_summary	"Distinct subsets of genes are differentially expressed between Oct4 and Ccna2-knockdown embryos, and indicated differential functions.  Further, a large panel of genes were confirmed to be differentially-expressed in Oct4-knockdown embryos by quantitative, real time RT-PCR."
GSE13992_series_matrix.txtimp_info.txt
HGF r is 6 
Found treated in !Series_overall_design	"For gene array analysis c-MetDhepa and c-MetloxP/loxP controls were stimulated for 2 hours with 2µg recombinant mouse HGF.Three animals per group were treated in parallel, before and after i.p. injection of recombinant HGF or NaCl."
GSE13992_series_matrix.txtimp_info.txt
HGF r is 8 
Found stimulated in !Series_overall_design	"For gene array analysis c-MetDhepa and c-MetloxP/loxP controls were stimulated for 2 hours with 2µg recombinant mouse HGF.Three animals per group were treated in parallel, before and after i.p. injection of recombinant HGF or NaCl."
GSE14006_series_matrix.txtimp_info.txt
Bmal1 r is 1 
Found mutant in !Series_summary	"Hair follicles undergo recurrent cycling of controlled growth (anagen), regression (catagen), and relative quiescence (telogen) with a defined periodicity. Taking a genomics approach to study gene expression during synchronized mouse hair follicle cycling, we discovered that, in addition to circadian fluctuation, CLOCK-regulated genes are also modulated in phase with the hair growth cycle. During telogen and early anagen, circadian clock genes are prominently expressed in the secondary hair germ, which contains precursor cells for the growing follicle. Analysis of Clock and Bmal1 mutant mice reveals a delay in anagen progression, and the secondary hair germ cells show decreased levels of phosphorylated Rb and lack mitotic cells, suggesting that circadian clock genes regulate anagen progression via their effect on the cell cycle. Consistent with a block at the G1 phase of the cell cycle, we show a significant upregulation of p21 in Bmal1 mutant skin. While circadian clock mechanisms have been implicated in a variety of diurnal biological processes, our findings indicate that circadian clock genes may be utilized to modulate the progression of non-diurnal cyclic processes."
GSE14021_series_matrix.txtimp_info.txt
Dyrk1a r is 1 
Found overexpression in !Series_summary	"The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. Mutation of a REST/NRSF binding site in the promoter of the REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1A-dosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the brain phenotypic changes that characterize DS, with an accessory role for the gene dosage imbalance of other chromosome 21 genes."
GSE14030_series_matrix.txtimp_info.txt
Dyrk1a r is 1 
Found overexpression in !Series_summary	"The molecular mechanisms that lead to the cognitive defects characteristic of Down syndrome (DS), the most frequent cause of mental retardation, have remained elusive. Here we use a transgenic DS mouse model to show that DYRK1A gene dosage imbalance deregulates chromosomal clusters of genes located near neuron-restrictive silencer factor (REST/NRSF) binding sites. We found that DYRK1A binds the SWI/SNF-complex known to interact with REST/NRSF. Mutation of a REST/NRSF binding site in the promoter of the REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1A-dosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the brain phenotypic changes that characterize DS, with an accessory role for the gene dosage imbalance of other chromosome 21 genes."
GSE14031-GPL5105_series_matrix.txtimp_info.txt
estrogen receptor r is 3 
Found knockout in !Series_title	"Global survey of miRNA profiles in the uterus and an estrogen receptor alpha knockout embryo"
GSE14031-GPL5106_series_matrix.txtimp_info.txt
estrogen receptor r is 3 
Found knockout in !Series_title	"Global survey of miRNA profiles in the uterus and an estrogen receptor alpha knockout embryo"
GSE14035_series_matrix.txtimp_info.txt
DM r is 6 
Found induced in !Series_overall_design	"In order to test this hypothesis, we studied streptozotocin-induced (STZ) type-1 DM and age-matched non-DM mice (n=6 to 10 per group in each experiment). Histological examination of femurs, collected from STZ-mice at 28-30 weeks from induction of DM or controls, showed remarkable differences in bone density and marrow composition. Bone marrow cells from healthy and diabetic animals were next selected for endothelial progenitors and cultured for 10 days under endothelial cell growth conditions. Next RNA was isolated and analysed by Illumina Sentrix Beadarrays."
GSE14071_series_matrix.txtimp_info.txt
AU r is 3 
Found stimulation in !Series_summary	"The inflammatory response plays out over time in a reproducible and organized manner after an initiating stimulus. Here we showed that the genes activated in cultured mouse fibroblasts in response to the proinflammatory cytokine tumor necrosis factor can be divided roughly into three groups, each with different induction kinetics. Whereas differential transcription is important in determining the grouping of these genes, differential mRNA stability also exerted strong influence in some cases overriding that of transcriptional control elements on the temporal order of gene expression. mRNA transcripts expressed early after TNF stimulation have abundant AU-rich elements in their 3'-untranslated regions whereas those expressed later are contain fewer AU-rich sequences. Thus mRNA stability and transcriptional control, two intrinsic characteristics of genes, control the kinetics of proinflammatory cytokine-induced gene expression."
GSE14072_series_matrix.txtimp_info.txt
Dyrk1a r is 1 
Found overexpression in !Series_summary	"REST/NRSF target gene L1cam modifies the transcriptional effect of Dyrk1Adosage imbalance on L1cam. DyrkA dosage imbalance perturbs Rest/Nrsf levels with decreased Rest/Nrsf expression in embryonic neurons and increased expression in adult neurons. We identified a coordinated deregulation of multiple genes that are responsible for the cellular phenotypic traits present in DS such as dendritic growth impairment and microcephaly during prenatal cortex development. Dyrk1a overexpression in primary mouse cortical neurons reduced the neuritic complexity. In the postnatal hippocampus, DYRK1A overexpression suppresses a form of synaptic plasticity that may be sufficient to cause DS cognitive defects. We propose that DYRK1A overexpression-related neuronal gene deregulation generates the"
GSE14088_series_matrix.txtimp_info.txt
Ube2m r is 7 
Found knockdown in !Series_overall_design	"Ube2m and Ube2f are E2 enzymes that direct protein modification by NEDD8. Here we explore the specific functions of Ube2f and Ube2m by comparing gene expression profiles following knockdown of their function in NIH 3T3 cells."
GSE14088_series_matrix.txtimp_info.txt
Ube2f r is 4 
Found knockdown in !Series_overall_design	"We used microarrays to detail the global programme of gene expression changes following knockdown of Ube2m and Ube2f in NIH 3T3 cells."
GSE14088_series_matrix.txtimp_info.txt
Ube2m r is 2 
Found knockdown in !Series_overall_design	"We used microarrays to detail the global programme of gene expression changes following knockdown of Ube2m and Ube2f in NIH 3T3 cells."
GSE14089_series_matrix.txtimp_info.txt
ASP r is 2 
Found treated in !Series_summary	"We determined the gene expression profiles of murine melan-a melanocytes treated with ASP or alpha-MSH over a 4 days time course using genome-wide oligonucleotide microarrays. As expected, the gene expression patterns emphasized the opposing effects of the 2 ligands, and there were significant reductions in expression of numerous melanogenic proteins elicited by ASP, which correlates with its inhibition of pigmentation. However, ASP also unexpectidly modulated the expression of genes involved in various other cellular pathways, including glutathione synthesis and redox metabolism. Many genes up-regulated by ASP are involved in morphogenesis, cell adhesion and ECM-receptor interactions."
GSE14089_series_matrix.txtimp_info.txt
alpha-MSH r is 4 
Found treated in !Series_summary	"We determined the gene expression profiles of murine melan-a melanocytes treated with ASP or alpha-MSH over a 4 days time course using genome-wide oligonucleotide microarrays. As expected, the gene expression patterns emphasized the opposing effects of the 2 ligands, and there were significant reductions in expression of numerous melanogenic proteins elicited by ASP, which correlates with its inhibition of pigmentation. However, ASP also unexpectidly modulated the expression of genes involved in various other cellular pathways, including glutathione synthesis and redox metabolism. Many genes up-regulated by ASP are involved in morphogenesis, cell adhesion and ECM-receptor interactions."
GSE14101_series_matrix.txtimp_info.txt
Mll r is 6 
Found knockdown in !Series_summary	"Leukemias with MLL-rearrangements are characterized by high expression of the homeo box gene MEIS1. In these studies, we knocked down Meis1 expression by shRNA lentivirus transduction in murine Mll-AF9 leukemia cells. Meis1 knockdown resulted in decreased proliferation and survival of murine Mll-AF9 leukemia cells. We also observed reduced clonogenic capacity and increased monocytic differentiation. The establishment of leukemia in transplant recipients was significantly delayed by Meis1 knockdown. Gene expression profiling of cells transduced with Meis1 shRNA showed reduced expression of genes associated with cell cycle entry and progression. shRNA mediated knockdown of MEIS1 in human MLL-fusion gene leukemia cell lines resulted in reduced cell growth. These results show that MEIS1 expression is important for MLL-rearranged leukemias and suggest that MEIS1 promotes cell cycle entry. Targeting MEIS1 may have therapeutic potential for treating leukemias expressing this transcription factor."
GSE14101_series_matrix.txtimp_info.txt
Meis1 r is 3 
Found expressing in !Series_overall_design	"Murine Mll-AF9 leukemia (4166) cells were transduced with lentivirus expressing shRNA against Meis1 or control lentivirus (empty vector). Gene expression profiles were compared at 48 hours post transduction, using Puromycin as selection agent for transduced cells."
GSE14201_series_matrix.txtimp_info.txt
de r is 8 
Found deletion in !Series_summary	"The small intestinal epithelium is the most rapidly self-renewing tissue of mammals. Proliferative cells are confined to crypts, while differentiated cell types predominantly occupy the villi. We recently demonstrated the existence of a long-lived pool of cycling stem cells defined by Lgr5 expression and intermingled with post-mitotic Paneth cells at crypt bottoms. We have now determined a gene signature for these so called Crypt Base Columnar (CBC) cells. One of the genes within this stem cell signature is the Wnt target Ascl2. Transgenic expression of the Ascl2 transcription factor throughout the intestinal epithelium induces crypt hyperplasia and de novo crypt formation on villi. Induced deletion of the Ascl2 gene in adult small intestine leads to disappearance of the CBC stem cells within days. The combined results from these gain- and loss-of-function experiments imply that Ascl2 controls intestinal stem cell fate."
GSE14201_series_matrix.txtimp_info.txt
Lgr5 r is 6 
Found expressing in !Series_overall_design	"For the stem cell signature we used cell fractions of intestines from Lgr5-EGFP-ires-CreERT2 mice, expressing GFP under the control of the Lgr5 promoter. RNA was isolated from two FACS sorted cell populations, one expressing GFP at high levels (GFPhi) and the other expressing GFP at low levels (GFPlo). For the analysis of Ascl2 target genes RNA was isolated from intestinal epithelial cells of Ah-Cre/Ascl2floxed/floxed animals and Ah-Cre/Ascl2floxed/wt control animals 3 and 5 days post induction. Differentially labelled cRNA from GFPhi and GFPlo cells from two different sorts (each combining three different mice) were hybridised on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in two dye swap experiments, resulting in four individual arrays. For the Ascl2 target gene analysis we analyzed the 3 and 5 days PI experiments in two dye swap experiments, resulting in four individual arrays."
GSE14216_series_matrix.txtimp_info.txt
Dnmt1 r is 5 
Found deficient in !Series_overall_design	"We compared gene expression patterns in Wildtype and DNA methylation deficient (Emx1-cre; Dnmt1 mutant) mouse dorsal cortex. We performed 3 replicates using different each individual mouse strain. The Sample GSM350992 table is the average log ratio for the 3 replicatesArrays were performed in triplicate."
GSE14216_series_matrix.txtimp_info.txt
Emx1 r is 2 
Found deficient in !Series_overall_design	"We compared gene expression patterns in Wildtype and DNA methylation deficient (Emx1-cre; Dnmt1 mutant) mouse dorsal cortex. We performed 3 replicates using different each individual mouse strain. The Sample GSM350992 table is the average log ratio for the 3 replicatesArrays were performed in triplicate."
GSE14216_series_matrix.txtimp_info.txt
Dnmt1 r is 1 
Found mutant in !Series_summary	"DNA methylation is a major epigenetic factor regulating genome reprogramming, cell differentiation, developmental gene expression.  To understand the role DNA methylation in CNS neurons, we generated conditional Dnmt1 mutant mice that possess ~90% hypomethylated cortical and hippocampal cells in the dorsal forebrain from E13.5 on.   The mutant mice were viable with a normal lifespan, but displayed severe neuronal cell death between E14.5 to 3-weeks postnatally.   Accompanied with the striking cortical and hippocampal degeneration, adult mutant mice exhibited neurobehavioral defects in learning and memory in adulthood.  Unexpectedly, a fraction of Dnmt1-/- cortical neurons survived through postnatal development, so that the residual cortex in mutant mice contained 20-30% of hypomethylated neurons throughout the life.  Hypomethylated excitatory neurons exhibited multiple defects in postnatal maturation including abnormal dendritic arborization and impaired neuronal excitability.  The mutant phenotypes are coupled with deregulation of those genes involved in neuronal layer-specification, cell death, and the function of ion channels.  Our results suggest that DNA methylation, through its role in modulating neuronal gene expression, plays multiple roles in regulating cell survival, neuronal migration and maturation in the CNS."
GSE14216_series_matrix.txtimp_info.txt
Dnmt1 r is 1 
Found mutant in !Series_overall_design	"We compared gene expression patterns in Wildtype and DNA methylation deficient (Emx1-cre; Dnmt1 mutant) mouse dorsal cortex. We performed 3 replicates using different each individual mouse strain. The Sample GSM350992 table is the average log ratio for the 3 replicatesArrays were performed in triplicate."
GSE14216_series_matrix.txtimp_info.txt
Emx1 r is 4 
Found mutant in !Series_overall_design	"We compared gene expression patterns in Wildtype and DNA methylation deficient (Emx1-cre; Dnmt1 mutant) mouse dorsal cortex. We performed 3 replicates using different each individual mouse strain. The Sample GSM350992 table is the average log ratio for the 3 replicatesArrays were performed in triplicate."
GSE14219_series_matrix.txtimp_info.txt
Sall4 r is 1 
Found null in !Series_title	"Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells"
GSE14219_series_matrix.txtimp_info.txt
peri r is 5 
Found null in !Series_summary	"Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells."
GSE14226_series_matrix.txtimp_info.txt
MMTV r is 8 
Found deficient in !Series_overall_design	"Hunk-deficient animals were crossed to mice harboring an MMTV-c-myc transgene (Leder et al., 1986).  Hunk heterozygous, MMTV-c-myc mice were backcrossed to Hunk heterozygous animals.  MMTV-c-myc female animals of each Hunk genotype were mated twice, then monitored twice weekly for mammary tumors.  Mice possessing tumors with a maximum diameter of 20 mm were sacrificed and organs were examined at necropsy.  Tumor nodules were identified by examination of organs through a Leica Wild MZ8 dissection microscope."
GSE14236_series_matrix.txtimp_info.txt
Flt3 r is 6 
Found expressing in !Series_overall_design	"We performed gene expression profiling: 32Dc vs. MLL-AF4 expressing 32Dc, 32Dc vs. Flt3 TKD+MLL-AF4 expressing 32Dc, and MLL-AF4 expressing 32Dc vs. Flt3 TKD+MLL-AF4 expressing 32Dc. A single sample for each expressing cells was analyzed."
GSE14242_series_matrix.txtimp_info.txt
Hyp r is 6 
Found activation in !Series_summary	"We used gene array analysis of cortical bone to identify Phex-dependent gene transcripts regulating Fgf23 production and mineralization in Hyp mice. We discovered that activation of Fgf receptor- and Wnt-pathways contribute to increased Ffg23 gene transcription in Hyp bone. We found evidence in Hyp bone for increased expression of Fgf1, Fgf7, and Egr2 in the Fgf-signaling pathway and decrements in Sost and Cpz and increments in Sfrp1 and 4 in the Wnt-signaling pathway. Moreover, activation of Fgf and Wnt-signaling stimulated, whereas Tgf β inhibited Fgf23 promoter activity in osteoblasts. We also observed reductions in Bmp1, a metalloproteinase that metabolizes the Fgf23 regulatory extracellular matrix protein Dmp1. These findings suggest that elevation of Fgf23 expression in osteocytes is regulated by interactions between cell surface expression of Phex, extracellular matrix proteins and paracrine effects of Fgf and Wnt. Alterations were also found in enzymes regulating the posttranslational processing and stability of Fgf23, including decrements in the glycosyltransferase Galnt3 and the proprotein convertase Pcsk5. In addition, we found that the Pcsk5 and the glycosyltransferase Galnt3 were decreased in Hyp bone, suggesting that reduced post-translational processing of FGF23 may also contribute to increased Fgf23 levels in Hyp mice. With regards to mineralization, we identified additional candidates to explain the intrinsic mineralization defect in Hyp osteoblasts, including increases in the mineralization inhibitors Mgp and Thbs4, as well as increases in local pH altering factors, carbonic anhydrase 12 (Car12) and 3 (Car3) and the sodium-dependent citrate transporter (Slc13a5). These studies demonstrate the complexity of gene expression alterations in bone that accompanies inactivating Phex mutations and identify novel pathways that may coordinate Fgf23 expression and mineralization of extracellular matrix in Hyp bone."
GSE14326_series_matrix.txtimp_info.txt
NRSF r is 1 
Found silencing in !Series_overall_design	"Agilent Whole Mouse Genome oligomicroarrays (GEO accession no. GPL2872, Agilent Technologies, Palo Alto, CA) were used. They contain 60-mer DNA probes synthesized in situ in a 44k format. Of 44,290 spots, 2756 are controls. The remaining 41,534 spots represent 33,661 unique transcripts which correspond to 20,202 unique human genes. Six independent (NRSF silencing overexpression, six individual samples) measurements were carried out for each group of biological conditions using exchanged dye-labeled RNA targets (i.e., Cy3 and Cy5 dyeswapping experiments)."
GSE14326_series_matrix.txtimp_info.txt
NRSF r is 2 
Found overexpression in !Series_overall_design	"Agilent Whole Mouse Genome oligomicroarrays (GEO accession no. GPL2872, Agilent Technologies, Palo Alto, CA) were used. They contain 60-mer DNA probes synthesized in situ in a 44k format. Of 44,290 spots, 2756 are controls. The remaining 41,534 spots represent 33,661 unique transcripts which correspond to 20,202 unique human genes. Six independent (NRSF silencing overexpression, six individual samples) measurements were carried out for each group of biological conditions using exchanged dye-labeled RNA targets (i.e., Cy3 and Cy5 dyeswapping experiments)."
GSE14336_series_matrix.txtimp_info.txt
p53 r is 1 
Found mutant in !Series_title	"Expression profiling of thymic lymphomas from p53 mutant (R270H) mice with varying HIF levels"
GSE14350_series_matrix.txtimp_info.txt
STAT5 r is 4 
Found deficient in !Series_summary	"Interleukin-2 receptor (IL-2R) signaling is essential for T regulatory (Treg) cell development and homeostasis. Here we show that expression of IL-2Rbeta chains that lack tyrosine residues important for the association of the adaptor Shc and the transcription factor STAT5 in IL-2Rbeta-deficient mice resulted in production of a normal proportion of natural Treg cells that suppressed severe autoimmunity related with deficiency in IL-2 or IL-2R. These mutant IL-2Rbeta chains supported suboptimal and transient STAT5 activation that upregulate the transcription factor Foxp3 to normal amounts in natural, but not induced, Treg cells. Using cells T cell obtained from normal C57BL/6 mice and mice harboring Treg cells with impaired IL-2R signaling, gene expression profiling revealed many targets in peripheral natural Treg cells that were IL-2-dependent and a substantial overlap between the Treg cell IL-2-dependent gene program and the Treg cell transcriptional signature. Collectively, these findings demonstrate that a critical, and perhaps minor, subset of IL-2-dependent targets in Treg cells is indexed to a low IL-2R signaling threshold and that a substantial proportion of the Treg cell gene program is regulated by IL-2. CD4 T effector cells also showed many IL-2R-dependent gene and these also overlapped in a distintive manner with the IL-2-dependent genes of Treg cells and the Treg gene signature."
GSE14350_series_matrix.txtimp_info.txt
Foxp3 r is 6 
Found activation in !Series_summary	"Interleukin-2 receptor (IL-2R) signaling is essential for T regulatory (Treg) cell development and homeostasis. Here we show that expression of IL-2Rbeta chains that lack tyrosine residues important for the association of the adaptor Shc and the transcription factor STAT5 in IL-2Rbeta-deficient mice resulted in production of a normal proportion of natural Treg cells that suppressed severe autoimmunity related with deficiency in IL-2 or IL-2R. These mutant IL-2Rbeta chains supported suboptimal and transient STAT5 activation that upregulate the transcription factor Foxp3 to normal amounts in natural, but not induced, Treg cells. Using cells T cell obtained from normal C57BL/6 mice and mice harboring Treg cells with impaired IL-2R signaling, gene expression profiling revealed many targets in peripheral natural Treg cells that were IL-2-dependent and a substantial overlap between the Treg cell IL-2-dependent gene program and the Treg cell transcriptional signature. Collectively, these findings demonstrate that a critical, and perhaps minor, subset of IL-2-dependent targets in Treg cells is indexed to a low IL-2R signaling threshold and that a substantial proportion of the Treg cell gene program is regulated by IL-2. CD4 T effector cells also showed many IL-2R-dependent gene and these also overlapped in a distintive manner with the IL-2-dependent genes of Treg cells and the Treg gene signature."
GSE14361_series_matrix.txtimp_info.txt
Sca-1 r is 5 
Found lacking in !Series_summary	"Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. "
GSE14361_series_matrix.txtimp_info.txt
FU r is 1 
Found exposure in !Series_summary	"Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. Upon injury these cells are induced to proliferate in order to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNα), HSCs efficiently exit G0 and enter an active cell cycle. HSCs respond to IFNα treatment by increased phosphorylation of STAT1 and PKB/Akt, expression of IFNα target genes and up-regulation of stem cell antigen-1 (Sca-1). HSCs lacking either the interferon-α/β receptor (IFNAR), STAT1 or Sca-1 are insensitive to IFNα stimulation, demonstrating that STAT1 and Sca-1 mediate IFNα induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-FU1, HSCs pre-treated (primed) with IFNα and thus induced to proliferate are efficiently eliminated by 5-FU exposure in vivo. Conversely, HSCs chronically activated by IFNα are functionally compromised and are rapidly out competed by non-activatable IFNAR-/- cells in competitive repopulation assays. In summary, while chronic activation of the IFNα pathway in HSCs impairs their function, acute IFNα treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNα on leukemic cells and raise the possibility for novel applications of type I interferons to target cancer stem cells. "
GSE14365_series_matrix.txtimp_info.txt
Aire r is 1 
Found deficient in !Series_title	"Expression data from WT and Aire deficient mTECs"
GSE14365_series_matrix.txtimp_info.txt
PHD r is 7 
Found deficient in !Series_summary	"Aire is an important transcription regulator that mediates a role in central tolerance via promoting the promiscuous expression of tissue-specific antigens in the thymus. Although several mouse models of Aire-deficiency have been described, none has analysed the phenotype induced by a mutation that emulates the common 13bp deletion in human APECED by disrupting the first PHD domain in exon 8. Aire-deficient mice with a corresponding mutation showed some disturbance of the medullary epithelial compartment, but at the phenotypic level their T cell compartment appeared relatively normal in the thymus and periphery. An increase in the number of activated T cells was evident, and autoantibodies against several organs were detected. At the histological level, lymphocytic infiltration of several organs indicated the development of autoimmunity, though symptoms were mild and quality of life for Aire-deficient mice appeared equivalent to wild-type littermates, with the exception of male infertility. Vbeta and CDR3 length analysis suggested that each Aire-deficient mouse developed it own polyclonal autoimmune repertoire. Finally, given the prevalence of candidiasis in APECED patients, we examined the control of infection with Candida albicans in Aire-deficient mice. No increase in disease susceptibility was found for either oral or systematic infection. These observations support the view that additional genetic and/or environmental factors contribute substantially to the overt nature of autoimmunity associated with Aire mutations, even for mutations identical to those found in humans with APECED."
GSE14365_series_matrix.txtimp_info.txt
Aire r is 1 
Found knock-out in !Series_overall_design	"In this experiment there are 5 samples altogether which consist of two biological replicates of Aire knock-out mTECs and 3 biological replicates of wild type mTECs."
GSE14365_series_matrix.txtimp_info.txt
PHD r is 8 
Found deletion in !Series_summary	"Aire is an important transcription regulator that mediates a role in central tolerance via promoting the promiscuous expression of tissue-specific antigens in the thymus. Although several mouse models of Aire-deficiency have been described, none has analysed the phenotype induced by a mutation that emulates the common 13bp deletion in human APECED by disrupting the first PHD domain in exon 8. Aire-deficient mice with a corresponding mutation showed some disturbance of the medullary epithelial compartment, but at the phenotypic level their T cell compartment appeared relatively normal in the thymus and periphery. An increase in the number of activated T cells was evident, and autoantibodies against several organs were detected. At the histological level, lymphocytic infiltration of several organs indicated the development of autoimmunity, though symptoms were mild and quality of life for Aire-deficient mice appeared equivalent to wild-type littermates, with the exception of male infertility. Vbeta and CDR3 length analysis suggested that each Aire-deficient mouse developed it own polyclonal autoimmune repertoire. Finally, given the prevalence of candidiasis in APECED patients, we examined the control of infection with Candida albicans in Aire-deficient mice. No increase in disease susceptibility was found for either oral or systematic infection. These observations support the view that additional genetic and/or environmental factors contribute substantially to the overt nature of autoimmunity associated with Aire mutations, even for mutations identical to those found in humans with APECED."
GSE14395_series_matrix.txtimp_info.txt
PPARalpha r is 4 
Found knock-out in !Series_overall_design	"Expression profile difference between male and female PPARalpha wild-type and knock-out mice in liver and heart (3 pools of 4 animals in each group). Wild-type (12 males and 12 females) and knock-out PPARalpha SV129 mice (12 males and 12 females) approximately 10 to 12 weeks of age were killed at ZT14 and their livers and hearts quickly removed and frozen."
GSE14395_series_matrix.txtimp_info.txt
PPAR-alpha r is 2 
Found KO in !Series_title	"Gender-specific gene repression of PPAR-alpha KO mice in liver and heart"
GSE14415_series_matrix.txtimp_info.txt
Foxp3 r is 8 
Found induced in !Series_summary	"We used gene expression microarrays to examine the transcriptional programs of natural and induced regulatory T cells and the function of Foxp3 in organizing the transcriptosomes of the respective cell type"
GSE14416_series_matrix.txtimp_info.txt
ICSBP r is 4 
Found expressing in !Series_overall_design	"Total RNA was isolated from parental BaF3 cells as well as BaF3 cells expressing BCR-ABL, ICSBP, or both BCR-ABL and ICSBP. Using standard Affymetrix protocols the RNA samples were analyzed for gene expression using Affymetrix mouse 430_2 whole genome microarrays arrays. A threshold value of 50 was set for all genes and the list of genes filtered to include only those that had at least one Present flag (""P"" flag) in one of the 4 conditions. For each gene, the ratio of its expression in a particular condition and its expression in parental BaF3 cells was determined. Only genes that had at least a 3-fold up or down change in expression were considered, leaving a set of 1431 genes for further analysis. K-means clustering with Gene cluster 3.0 was used to group these 1431 genes into 15 clusters and JavaTree was used to visualize the results."
GSE14418_series_matrix.txtimp_info.txt
IgG r is 4 
Found treated in !Series_overall_design	"Cy3: B16F10 mouse melanoma cells, treated by unspecific goat IgG (control) for 2 hours."
GSE14418_series_matrix.txtimp_info.txt
TIM r is 2 
Found stimulation in !Series_title	"The effect of TIM-3 stimulation on the gene expression profile of B16-F10 melanoma cells"
GSE14418_series_matrix.txtimp_info.txt
F10 r is 8 
Found stimulation in !Series_title	"The effect of TIM-3 stimulation on the gene expression profile of B16-F10 melanoma cells"
GSE14418_series_matrix.txtimp_info.txt
TIM-3 r is 2 
Found stimulation in !Series_title	"The effect of TIM-3 stimulation on the gene expression profile of B16-F10 melanoma cells"
GSE14418_series_matrix.txtimp_info.txt
TIM r is 2 
Found stimulation in !Series_summary	"The effect of TIM-3 stimulation was studied on B16F10 mouse melanoma cells, in vitro."
GSE14418_series_matrix.txtimp_info.txt
TIM-3 r is 2 
Found stimulation in !Series_summary	"The effect of TIM-3 stimulation was studied on B16F10 mouse melanoma cells, in vitro."
GSE14430_series_matrix.txtimp_info.txt
pancreatic polypeptide r is 5 
Found loss of in !Series_summary	"Glis3 mutant mice (Glis3zf/zf) die within the first week after birth due to overt diabetes, evidenced by hyperglycemia and hypoinsulinemia. Histopathological analysis showed that Glis3zf/zf mice develop a pancreatic phenotype with a dramatic loss of beta- (insulin) and delta- (somatostatin) cells contrasting a smaller relative loss of alpha- (glucagon), PP- (pancreatic polypeptide), and epsilon- (ghrelin) cells. Glis3zf/zf mice develop ductal cysts with decreased number of primary cilia, while the acini are not significantly affected. Gene expression profiling by microarray analysis demonstrated that the expression of terminal hormonal genes and several transcription factors important in endocrine development were significantly deregulated in Glis3zf/zf mice. During pancreatic development, Glis3 mRNA expression is induced during the secondary transition, a stage of cell lineage specification and extensive patterning. Changes in pancreatic development of Glis3zf/zf mice are noted during and after this stage; the number of cells staining positively for Ngn3, MafA, or Pdx-1 is greatly diminished. These observations indicate that Glis3 plays a key role in the development of mature beta cells."
GSE14430_series_matrix.txtimp_info.txt
Glis3 r is 4 
Found induced in !Series_summary	"Glis3 mutant mice (Glis3zf/zf) die within the first week after birth due to overt diabetes, evidenced by hyperglycemia and hypoinsulinemia. Histopathological analysis showed that Glis3zf/zf mice develop a pancreatic phenotype with a dramatic loss of beta- (insulin) and delta- (somatostatin) cells contrasting a smaller relative loss of alpha- (glucagon), PP- (pancreatic polypeptide), and epsilon- (ghrelin) cells. Glis3zf/zf mice develop ductal cysts with decreased number of primary cilia, while the acini are not significantly affected. Gene expression profiling by microarray analysis demonstrated that the expression of terminal hormonal genes and several transcription factors important in endocrine development were significantly deregulated in Glis3zf/zf mice. During pancreatic development, Glis3 mRNA expression is induced during the secondary transition, a stage of cell lineage specification and extensive patterning. Changes in pancreatic development of Glis3zf/zf mice are noted during and after this stage; the number of cells staining positively for Ngn3, MafA, or Pdx-1 is greatly diminished. These observations indicate that Glis3 plays a key role in the development of mature beta cells."
GSE14438_series_matrix.txtimp_info.txt
IgG r is 5 
Found treated in !Series_overall_design	"Bone marrow cells were differentiated in RPMI + 10% FCS + 5 ng/ml mouse IL-3 + 40 ng/ml mouse SCF for >4 weeks. The purity of the cell cultures was >90% at this time point (FcERIa+/c-kit+ cells). These in vitro-differentiated immature mast cells were then treated by either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml for 2 or 16 hours). For the IgE/antigen-activated mouse mast cells, these in vitro-differentiated immature mast cells were sensitized by 5 ug/ml anti-DNP IgE (Sigma) for 1 hour and then treated with 100 ng/ml DNP-HSA (antigen, Sigma) and either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml) for 2 or 16 hours. The anti-TIM-3 samples were labeled by Cy5 and they were compared to the Cy3-labeled, goat IgG controls in a dual-color, paired experimental setup. The Agilent Whole Mouse Genome 4x44K expression microarray kit and Dual-Color Protocol version 5.5 were used in the experiments."
GSE14438_series_matrix.txtimp_info.txt
TIM r is 2 
Found stimulation in !Series_title	"The effect of TIM-3 stimulation on the gene expression profile of IgE/antigen-activated mouse mast cells"
GSE14438_series_matrix.txtimp_info.txt
TIM-3 r is 2 
Found stimulation in !Series_title	"The effect of TIM-3 stimulation on the gene expression profile of IgE/antigen-activated mouse mast cells"
GSE14454_series_matrix.txtimp_info.txt
Eps8 r is 3 
Found knockout in !Series_summary	"In a variety of organisms, including mammals, caloric restriction improves metabolic status and lowers the incidence of chronic-degenerative diseases, ultimately leading to increased lifespan. Here we show that knockout mice for Eps8, a regulator of actin dynamics, display reduced bodyweight, partial resistance to age- or diet-induced obesity, and overall improved metabolic status. We present evidence that these phenotypes, which are associated to increased lifespan in the Eps8 null mice, are due to caloric restriction. This, in turn, is caused by reduced intestinal fat absorption, due to altered morphogenesis of microvilli in intestinal enterocytes. In the nematode, genetic removal of Eps8, causes a microvillar phenotype, indistinguishable from that observed in mice, which leads to early larval lethality. By exploiting the nematode model system, we demonstrate here that the actin bundling activity of Eps8 is indispensable for viability and proper intestinal morphogenesis. This result links a precise molecular function of Eps8 to proper microvillar morphogenesis, and therefore to the phenotype of Eps8-null mice. Our results implicate actin dynamics in individual variations in bodyweight, metabolic status and longevity."
GSE14457-GPL2881_series_matrix.txtimp_info.txt
p53 r is 1 
Found mutant in !Series_summary	"The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss."
GSE14457-GPL2881_series_matrix.txtimp_info.txt
mutant p53 r is 0 
Found mutant in !Series_summary	"The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss."
GSE14457-GPL4092_series_matrix.txtimp_info.txt
p53 r is 1 
Found mutant in !Series_summary	"The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss."
GSE14457-GPL4092_series_matrix.txtimp_info.txt
mutant p53 r is 0 
Found mutant in !Series_summary	"The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss."
GSE14457-GPL891_series_matrix.txtimp_info.txt
p53 r is 1 
Found mutant in !Series_summary	"The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss."
GSE14457-GPL891_series_matrix.txtimp_info.txt
mutant p53 r is 0 
Found mutant in !Series_summary	"The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss."
GSE14470_series_matrix.txtimp_info.txt
p53 r is 3 
Found -/- in !Series_overall_design	"Samples: purified CGNP-like mouse medulloblastoma cells; purified CGNPs from age day 6 (P6) mice; whole cerebellum from P6 mice; whole cerebellum from 1 month old mice.  Each from three backgrounds (except tumors)  - wt; Ptc+/-,Ink4c-/-; p53-/-,Ink4c-/-.  Two to five biological replicates each."
GSE14512_series_matrix.txtimp_info.txt
MuRF1 r is 2 
Found -/- in !Series_overall_design	"Four strain-matched groups of 12 week old mice were investigated: 1) MuRF1 -/- MuRF2 -/-; 2) MuRF1 +/+ MuRF2 +/+; 3) MuRF1 -/- MuRF2 +/-; 4) MuRF1 +/- MuRF2 -/-.  Biological replicates:  4 WT, 4 MuRF1 -/- // MuRF2 -/-, 4 MuRF1 +/- //MuRF2 -/-, 4 MuRF1 -/- // MuRF2 +/-.  Hearts harvested.  One replicate per array."
GSE14525_series_matrix.txtimp_info.txt
MLCK r is 1 
Found knockout in !Series_summary	"Acute lung injury (ALI), a major cause of acute respiratory failure with high morbidity and mortality, isare characterized by significant pulmonary inflammation and both alveolar and vascular barriers dysfunction.  In Pprior studies have highlighted the role of nonmuscle myosin light chain kinase (nmMLCK) as an essential element of inflammatory response with MYLK polymorphisms associated withwhich alters ALI susceptibility. In the present study we sought to further define nmMLCK in acute inflammatory syndromes and examined We examined nmMLCK as a molecular target involved in increase of lung epithelial and endothelial barrier permeability. We utilized in two muirine models of inflammatory lung injury: intratracheal administration of endotoxin/lipopolysaccharide (LPS, 2.5 mg/kg) and VILI (ventilator-induced lung injury, tidal volume 40ml/kg).  Two complementary strategies were used to reduce nmMLCK activity or expression. We found that membrane permeant oligopeptide, PIK, inhibited MLC kinase activity in vitro in aand displayed dose-dependent mannerinhibition of MLC kinase activity.. Intravenous delivery of PIK significantly attenuated LPS-induced lung inflammation reflected by decreasing accumulation of bronchoalveolar lavage (BAL) albumin (~ 50% reduction) as well as reduction in BAL cells, tissue MPO activity and tissue albumin in lung homogenates. A second regulatory approach explored targeting murine nmMLCK by administration of siRNA (5mg/kg) 3 days prior to LPS challenge. siRNA decreased of nmMLCK expression in lungs (~ 70% reduction) and resulted in significant attenuation LPS-induced lung inflammation (~ 40% reduction) as reflected by decreased BAL protein level and BAL cells. For targeting pulmonary vessels nmMLCK we used ACE antibody-conjugated liposomes with nmMLCK siRNA in murine ventilator-induced lung injury (VILI) model. Protein silencing of nmMLCK was evident by immunohistochemical analysis with a decrease in relative intensity of fluorescence in lung vessels compared with control animals. Furthermore, the inhibition of nmMLCK expression by siRNA in vessels significantly attenuated VILI lung injury as reflected by decreased BAL protein level (40% reduction). Finally, MLCK knockout mice were significantly protected (reduced BAL protein and albumin) when exposed to a model of severe VILI (4h, 40ml/kg tidal volume). Conclusion: the MLCK gene KO and chemical biology results indicate that the targeting of nmMLCK in vivo attenuate the severity of LPS-induced or VILI acute lung injury."
GSE14536_series_matrix.txtimp_info.txt
AP-2 r is 2 
Found mutant in !Series_overall_design	"Biological triplicates of mouse lenses were analyzed (three wild-type lens samples and three Le-AP-2 mutant samples)"
GSE14539_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found knockout in !Series_summary	"Surgical resection is the preferred treatment for Hepatocellular carcinoma; however, it induces tumor recurrence. Our objective was to understand the molecular mechanisms linking liver regeneration under chronic-inflammation to tumorigenesis. Mdr2-knockout mice, a model of inflammation-associated cancer, underwent partial-hepatectomy which led to enhanced hepatocarcinogenesis. Yet, liver regeneration in these mice was severely attenuated. We demonstrate the activation of the DNA damage response machinery and altered genomic instability during early liver inflammatory stages resulting in hepatocyte apoptosis and cell-cycle arrest, and suggest their involvement in tumor recurrence subsequent to partial hepatectomy. We propose that under the regenerative proliferative stress induced by liver resection, the genomic unstable hepatocytes generated during chronic-inflammation, escape apoptosis and reenter the cell-cycle, triggering the enhanced tumorigenesis"
GSE14539_series_matrix.txtimp_info.txt
Mdr2 r is 1 
Found -/- in !Series_overall_design	"RNA was isolated from liver samples of 9-month-old Mdr2-/- and control mice obtained on days 0 (the removed lobe), 2 and 6 following PHx. Samples of d0 were obtained from the same mice that were sacrificed on later days. As we were concerned by the variability in the KO group 6 samples were obtained for d0. All other time points and groups contained 3 samples each."
GSE14549_series_matrix.txtimp_info.txt
Wrn r is 1 
Found mutant in !Series_title	"Gene expression profiling in liver of mice with a mutant Wrn protein treated with/without vitamin C compared to WT mice."
GSE14549_series_matrix.txtimp_info.txt
Wrn r is 1 
Found mutant in !Series_summary	"Werner syndrome (WS) is a rare disorder characterized by the premature onset of a number of age-related diseases. The gene responsible for WS is believed to be involved in different aspects of transcription, replication, and/or DNA repair. We generated a mouse model with a deletion in the helicase domain of the murine WRN homologue that recapitulates most of the WS phenotypes including an abnormal hyaluronic acid excretion, higher reactive oxygen species (ROS) levels, increased genomic instability and cancer incidence resulting in a 10-15% decreased life span expectancy. In addition, WS patients and Wrn mutant mice show hallmarks of a metabolic syndrome including premature visceral obesity, hypertriglyceridemia, insulin-resistant diabetes type 2 and associated cardiovascular diseases. In this study, we compared the expression profile of liver tissues from 9 months old Wrn mutant and wild type animals. Gene set enrichment analysis of the microarray data indicated that Wrn mutant mice exhibited down-regulation of genes normally decreased in several transgenic mouse models of hepatoma and during caloric restriction. Wrn mutant mice also altered the expression of genes involved in inflammation as well as in glutathione and xenobiotic metabolisms. These results indicate that Wrn mutant mice respond to the observed oxidative stress by altering the necessary pathways to survive. Vitamin C supplementation rescued the life span expectancy of Wrn mutant mice and reversed several age-related abnormalities in adipose, cardiac, and liver tissues, genomic integrity and inflammatory status. Finally, gene set enrichment analyses revealed that vitamin C decreased genes normally up regulated in human WS fibroblasts and cancers and it increased genes involved in tissue injury response and adipocyte dedifferentiation in obese mice."
GSE14549_series_matrix.txtimp_info.txt
Wrn r is 1 
Found mutant in !Series_overall_design	"Microarray analyses were performed on the liver tissues of 9 months old mice. Four independent biological replicates of this experiment (wild type vs Wrn mutant or wild type vs vitamin C treated mutant mice) were carried out with a dye swap on two replicates of each genotype."
GSE14549_series_matrix.txtimp_info.txt
Wrn r is 2 
Found treated in !Series_title	"Gene expression profiling in liver of mice with a mutant Wrn protein treated with/without vitamin C compared to WT mice."
GSE14549_series_matrix.txtimp_info.txt
Wrn r is 8 
Found treated in !Series_overall_design	"Microarray analyses were performed on the liver tissues of 9 months old mice. Four independent biological replicates of this experiment (wild type vs Wrn mutant or wild type vs vitamin C treated mutant mice) were carried out with a dye swap on two replicates of each genotype."
GSE14550_series_matrix.txtimp_info.txt
podoplanin r is 1 
Found overexpressing in !Series_title	"Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin (human array)"
GSE14551_series_matrix.txtimp_info.txt
podoplanin r is 1 
Found overexpressing in !Series_title	"Gene expression profiling of tumor stroma of MCF7 breast cancer xenografts overexpressing podoplanin (mouse array)"
GSE14559_series_matrix.txtimp_info.txt
IP r is 8 
Found induced in !Series_summary	"To decipher the structure and behaviors of the transcription factor (TF) network, we created 50 permanent mouse ES cell lines, in each of which one of the 50 transcription factors tagged with FLAG, is inserted into the doxycycline (dox)-repressible ROSA26 locus. Expression profiling reveals Cdx2 as the most potent inducer of transcriptome perturbation in ES cells, followed by Esx1, Sox9, Tcf3, Klf4, and Gata3. Immunoprecipitation (IP) with a FLAG-antibody in Cdx2-induced ES cells, identifies NuRD in CDX2-associated protein complexes; and chromatin-IP-sequencing identifies CDX2-binding sites predominantly in genes up-regulated by CDX2. Compendium analyses of Cdx2- and the other TF-inducible ES cells suggest a central role of the POU5F1/SOX2/NANOG protein complex in a swift-acting control mechanism to down-regulate a common set of genes at the beginning of multi-lineage ES cell differentiations. These ES cell lines will be a valuable resource to study biological networks in ES cells and mice."
GSE14561_series_matrix.txtimp_info.txt
Pig r is 2 
Found knock-out in !Series_summary	"Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion."
GSE14561_series_matrix.txtimp_info.txt
Pig-a r is 2 
Found knock-out in !Series_summary	"Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion."
GSE14561_series_matrix.txtimp_info.txt
Pig r is 2 
Found knock-out in !Series_overall_design	"We performed microarray analysis on 3 pools of sorted GPI-deficient (GPI-) and GPI normal (GPI+) bone marrow cells derived from the same Pig-a knock-out animals, and identified 1275/669 genes of the 45,101 transcripts potentially available for screening using 2-fold change, <10% false discovery rate (FDR) and percentage of present calls as selection criteria. The major representative genes belong to the category of immune response. We tested whether the molecular differences between GPI- and GPI+  bone marrow cells could be preserved when GPI- cells were transplanted in lethally-irradiated wild type mice (C57BL/6). Microarray analysis was performed using sorted bone marrow cells from 4 animals transplanted with GPI-deficient bone marrow cells (T-GPI-) from Pig-a knock-out donors, 3 animals transplanted with GPI-normal bone marrow cells from C57BL/6 donors (T-GPI+), and  GPI-normal bone marrow cells from 4  wild-type C57BL/6 mice (WT-GPI+). We found 296 probesets with  2-fold change cutoff, of which T-GPI- cells had 145 up-regulated genes in comparison to WT-GPI+ cells, and had 123 genes differentially expressed when compared to T-GPI+ cells. The gene expression of the GPI-deficient cells was very similar between the two sets of microarray experiments affirming the maintenance of the phenotype before and after bone marrow cell transplantation."
GSE14561_series_matrix.txtimp_info.txt
Pig-a r is 2 
Found knock-out in !Series_overall_design	"We performed microarray analysis on 3 pools of sorted GPI-deficient (GPI-) and GPI normal (GPI+) bone marrow cells derived from the same Pig-a knock-out animals, and identified 1275/669 genes of the 45,101 transcripts potentially available for screening using 2-fold change, <10% false discovery rate (FDR) and percentage of present calls as selection criteria. The major representative genes belong to the category of immune response. We tested whether the molecular differences between GPI- and GPI+  bone marrow cells could be preserved when GPI- cells were transplanted in lethally-irradiated wild type mice (C57BL/6). Microarray analysis was performed using sorted bone marrow cells from 4 animals transplanted with GPI-deficient bone marrow cells (T-GPI-) from Pig-a knock-out donors, 3 animals transplanted with GPI-normal bone marrow cells from C57BL/6 donors (T-GPI+), and  GPI-normal bone marrow cells from 4  wild-type C57BL/6 mice (WT-GPI+). We found 296 probesets with  2-fold change cutoff, of which T-GPI- cells had 145 up-regulated genes in comparison to WT-GPI+ cells, and had 123 genes differentially expressed when compared to T-GPI+ cells. The gene expression of the GPI-deficient cells was very similar between the two sets of microarray experiments affirming the maintenance of the phenotype before and after bone marrow cell transplantation."
GSE14585_series_matrix.txtimp_info.txt
Xist r is 3 
Found silencing in !Series_summary	"The non-coding Xist RNA triggers silencing of one of the two female X chromosomes during X inactivation in mammals. Gene silencing by Xist is restricted to special developmental contexts found in cells of the early embryo and specific hematopoietic precursors. The absence of critical silencing factors might explain why Xist cannot silence outside these contexts. Here, we show that Xist can also initiate silencing in a lymphoma model. Using the tumor context we identify the special AT rich binding protein SATB1 as an essential silencing factor. We show that loss of SATB1 in tumor cells abrogates the silencing function of Xist. In normal female lymphocytes Xist localizes along SATB1 filaments and, importantly, forced Xist expression can relocalize SATB1 into the Xist cluster. This reciprocal influence on localization suggests a molecular interaction between Xist and SATB1. SATB1 and its close homologue SATB2 are expressed during the initiation window for X inactivation in embryonic stem cells and are recruited to surround the Xist cluster. Furthermore, ectopic expression SATB1 or SATB2 enables gene silencing by Xist in embryonic fibroblasts, which normally do not provide an initiation context. Thus, SATB1 functions as a crucial initiation factor and may act to organize genes for silencing by Xist during the initiation of X inactivation."
GSE14586_series_matrix.txtimp_info.txt
Cdx2 r is 1 
Found overexpression in !Series_summary	"(F) Potential CDX2-direct target genes based on ChIP-Seq and the alteration of expression by Cdx2-overexpression."
GSE14605_series_matrix.txtimp_info.txt
Ago2 r is 6 
Found knockout in !Series_overall_design	"gene expression profiling from two single wild-type oocytes, two single Dicer knockout oocyte, and one single Ago2 knockout oocyte"
GSE14654_series_matrix.txtimp_info.txt
LAP r is 7 
Found expressing in !Series_summary	"To study the function of Paf1C in mouse ESCs, we generated an ES cell line stably expressing a location and affinity purification (LAP)-tagged Ctr9 fusiuon protein using the bacterial astificial chromosome (BAC)-based TransgeneOmics approach. To investigate whether pluripotency and lineage control genes differentially regulated upon Paf1C depletion are direct targets of the Paf1C, we analyzed the binding of the Ctr9-LAP fusion protein by ChIP-chip and identified 2175 promoter regions that were bound by Ctr9."
GSE14672_series_matrix.txtimp_info.txt
Stat5a r is 2 
Found lacking in !Series_summary	"GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B.  To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells.  Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. GMPs were isolated and cultured with GM-CSF.  Both the number and size of STAT5A/B-null colonies were reduced and GM-CSF-induced survival of mature STAT5A/B-null neutrophils was impaired.  Time-lapse cinematography and single cell tracking of GMPs revealed that STAT5A/B-null cells were characterized by a longer generation time and an increased cell death.  Gene expression profiling experiments suggested that STAT5A/B directs GM-CSF signaling through the regulation of cell survival genes."
GSE14672_series_matrix.txtimp_info.txt
Stat5a r is 5 
Found lacking in !Series_overall_design	"Mice lacking or with  the Stat5a and 5b genes in blood cells, which were treated w/o GMP"
GSE14691-GPL1261_series_matrix.txtimp_info.txt
Clcn1 r is 1 
Found null in !Series_overall_design	"All experiments involved generating expression profiles of quadriceps muscles taken from mice. Experiments 1 and 2: samples were hybridized to Moe430A and Moe430B arrays. Experiment 3: samples were hybridized to Mouse Genome 430 2.0 array. Experiment 1 compared expression profiles of wild-type mice (FVB strain) with two lines, designated 20b and 41, of CUGexp transgenic mice with FVB background. Experiment 2 compared expression profiles of Clcn1-null (myotonic) mice with the wild-type background strain (BALB). Experiment 3 compared expression profiles of Mbnl1-null mice with the wild-type background strain (FVB)."
GSE14691-GPL339_series_matrix.txtimp_info.txt
Clcn1 r is 1 
Found null in !Series_overall_design	"All experiments involved generating expression profiles of quadriceps muscles taken from mice. Experiments 1 and 2: samples were hybridized to Moe430A and Moe430B arrays. Experiment 3: samples were hybridized to Mouse Genome 430 2.0 array. Experiment 1 compared expression profiles of wild-type mice (FVB strain) with two lines, designated 20b and 41, of CUGexp transgenic mice with FVB background. Experiment 2 compared expression profiles of Clcn1-null (myotonic) mice with the wild-type background strain (BALB). Experiment 3 compared expression profiles of Mbnl1-null mice with the wild-type background strain (FVB)."
GSE14691-GPL340_series_matrix.txtimp_info.txt
Clcn1 r is 1 
Found null in !Series_overall_design	"All experiments involved generating expression profiles of quadriceps muscles taken from mice. Experiments 1 and 2: samples were hybridized to Moe430A and Moe430B arrays. Experiment 3: samples were hybridized to Mouse Genome 430 2.0 array. Experiment 1 compared expression profiles of wild-type mice (FVB strain) with two lines, designated 20b and 41, of CUGexp transgenic mice with FVB background. Experiment 2 compared expression profiles of Clcn1-null (myotonic) mice with the wild-type background strain (BALB). Experiment 3 compared expression profiles of Mbnl1-null mice with the wild-type background strain (FVB)."
GSE14698_series_matrix.txtimp_info.txt
Stat5a r is 5 
Found lacking in !Series_title	"Microarray Experiments for mice lacking or with  the Stat5a and 5b genes in blood cells that were treated w/o CMP"
GSE14698_series_matrix.txtimp_info.txt
Stat5a r is 2 
Found lacking in !Series_summary	"GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B.  To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells.  Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. CMPs were isolated and cultured with GM-CSF.  "
GSE14698_series_matrix.txtimp_info.txt
Stat5a r is 5 
Found lacking in !Series_overall_design	"Microarray Experiments for mice lacking or with  the Stat5a and 5b genes in blood cells that were treated w/o CMP"
GSE14699_series_matrix.txtimp_info.txt
BH3-only r is 7 
Found deletion in !Series_summary	"Consistent with defective cytolysis, these cells exhibited deficiencies in granzyme up-regulation. Furthermore, they showed antigen-driven Bcl-2 down-regulation and early up-regulation of the pro-apoptotic protein Bim, consistent with the requirement of this BH3-only protein for peripheral T cell deletion. Bim up-regulation was paralleled by defective IL-7Ra chain re-expression, suggesting that Bim-dependent death may be triggered by loss of IL-7/IL-7R signaling. Finally, we observed parallels in molecular signatures between deletion and anergy suggesting that these tolerance pathways may not be as molecularly distinct as previously surmised."
GSE14710_series_matrix.txtimp_info.txt
GH r is 2 
Found stimulation in !Series_summary	"In skeletal muscle, STAT5a/b transcription factors are critical for normal postnatal growth, whole-animal glucose homeostasis, and local IGF-1 production.  These observations have led us to hypothesize that STAT5a/b are critical for maintenance of normal muscle mass and function.  To investigate this, mice with a skeletal muscle-specific deletion of the Stat5a/b genes (Stat5MKO) were used.  Stat5MKO mice displayed reduced muscle mass, altered fiber-type distribution and reduced activity.  On a molecular level, gene expression in skeletal muscle of Stat5MKO and control mice was analyzed by microarrays and real-time PCR, both in the presence and absence of growth hormone (GH) stimulation.  Several genes involved in muscle growth, fiber-type and metabolism were significantly changed.  Specifically in the quadriceps, a muscle almost exclusively composed of type II fibers, the absence of STAT5a/b led to increased expression of several genes associated with type I fibers and the de novo appearance of type I fibers.  Additionally, it is shown here that expression of the androgen receptor gene (Ar) is controlled by GH through STAT5a/b.  The link between STAT5a/b and Ar gene is likely through direct transcriptional regulation, as chromatin immunoprecipitaion of the Ar promoter region in C2C12 myoblasts was accomplished by antibodies against STAT5a. These experiments demonstrate an important role for STAT5a/b in skeletal muscle physiology and they provide a direct link to androgen signaling."
GSE14800_series_matrix.txtimp_info.txt
Lasp1 r is 2 
Found loss of in !Series_summary	"Chronic loss of Lasp1 alters the expression of other genes associated with cell motility/attachment, and/or other cellular functions.  Results provide new information showing that loss of Lasp1 leads to up- and down-regulation of genes involved in cell motility/attachment/growth."
GSE14800_series_matrix.txtimp_info.txt
Lasp1 r is 1 
Found -/- in !Series_overall_design	"Total RNA isolated from  Lasp1-/- MEFs compared to Lasp1+/+ MEFs."
GSE14813_series_matrix.txtimp_info.txt
Lasp1 r is 1 
Found null in !Series_summary	"Comparative analysis of gene expression in murine gastric fundic mucosa in wild-type and Lasp1-null littermates. The data provide a comprehensive overview of genes expressed in the mouse gastric mucosa and show that the expression of several known and unidentified genes is modified by disruption of the Lasp1 gene."
GSE14829_series_matrix.txtimp_info.txt
ras r is 1 
Found knockout in !Series_summary	"The similarity of transcription profiles among serum-starved fibroblasts of all different WT and ras knockout genotypes tested, indicated that H-Ras and N-Ras do not play significant roles in control of transcriptional responses to serum deprivation stress. In contrast, genomic disruption of H-ras or N-ras, individually or in combination, determined highly specific, differential gene expression profiles in response to post-starvation stimulation with serum for 1 hour (G0/G1 transition) or for 8 hours (mid-G1 progression). The absence of N-Ras caused significantly higher changes than the absence of H-Ras on the wave of transcriptional activation linked to G0/G1 transition. In contrast, the absence of H-Ras affected more potently the profile of the transcriptional wave detected during mid-G1 progression. Functional analysis demonstrated a predominant functional association of H-Ras with growth and proliferation, whereas N-Ras exhibited a closer functional link to development or cell cycle regulation as well as immunomodulation and apoptosis. Mechanistic analysis indicated that ERK-dependent activation of Stat1 mediates the regulatory effect of N-Ras on defense and immunity, whereas the pro-apoptotic effects of N-Ras are mediated through ERK and p38 signaling.  Our observations support previous reports of an absolute requirement for different peaks of Ras activity during the initial stages of the cell cycle and confirm the notion of functional specificity for the H-Ras and N-Ras isoforms."
GSE14829_series_matrix.txtimp_info.txt
H-ras r is 6 
Found knockout in !Series_summary	"The similarity of transcription profiles among serum-starved fibroblasts of all different WT and ras knockout genotypes tested, indicated that H-Ras and N-Ras do not play significant roles in control of transcriptional responses to serum deprivation stress. In contrast, genomic disruption of H-ras or N-ras, individually or in combination, determined highly specific, differential gene expression profiles in response to post-starvation stimulation with serum for 1 hour (G0/G1 transition) or for 8 hours (mid-G1 progression). The absence of N-Ras caused significantly higher changes than the absence of H-Ras on the wave of transcriptional activation linked to G0/G1 transition. In contrast, the absence of H-Ras affected more potently the profile of the transcriptional wave detected during mid-G1 progression. Functional analysis demonstrated a predominant functional association of H-Ras with growth and proliferation, whereas N-Ras exhibited a closer functional link to development or cell cycle regulation as well as immunomodulation and apoptosis. Mechanistic analysis indicated that ERK-dependent activation of Stat1 mediates the regulatory effect of N-Ras on defense and immunity, whereas the pro-apoptotic effects of N-Ras are mediated through ERK and p38 signaling.  Our observations support previous reports of an absolute requirement for different peaks of Ras activity during the initial stages of the cell cycle and confirm the notion of functional specificity for the H-Ras and N-Ras isoforms."
GSE14855_series_matrix.txtimp_info.txt
MnSOD r is 1 
Found knockout in !Series_title	"Effect of MnSOD knockout cells on gene profile expression"
GSE14855_series_matrix.txtimp_info.txt
nt r is 5 
Found silencing in !Series_overall_design	"WT-AML-12 cells silenced (si) for MnSOD were prepared, briefly: The backbone vector pSUPER.retro.puro was used for silencing. Transcripts of 60-nt long oligos constituting hairpin RNAs were designed to generate a low level of MnSOD silencing: a nine-loop (9 L) hairpin with 20 nt of MnSOD sense (siMnSOD) and a 9 L hairpin with 20 nt of scramble-no gene recognition control sense (Scr). Retroviral particles were produced by triple transfection of HEK 293T cells (ATCC No. CRL-11268T) with the retroviral vector (2 ug), pMD-gag-pol (1 ug) and pVSV-G (1 ug) using Trans-IT (Mirusbio Corporation, Madison, WI). For stable transfection, the various retroviruses were introduced with WT-AML-12 hepatocytes using polybrene (Sigma-Aldrich, St. Louis, MO, USA) in a six-well plate followed by selection with 10 ug puromycin for 2 weeks."
GSE14862_series_matrix.txtimp_info.txt
Rag1 r is 1 
Found -/- in !Series_summary	"Intestinal ischemia-reperfusion (IR) injury is initiated when natural IgM antibodies recognize neo-epitopes that are revealed on ischemic cells. The target molecules and mechanisms whereby these neo-epitopes become accessible to recognition are not well understood. Proposing that isolated intestinal epithelial cells (IEC) may carry IR-related neo-epitopes, we used in vitro IEC binding assays to screen hybridomas created from B cells of unmanipulated wild type C57BL/6 mice. We identified a novel IgM monoclonal antibody (mAb B4) that reacted with the surface of IEC by flow cytometric analysis and was alone capable of causing complement activation, neutrophil recruitment and intestinal injury in otherwise IR-resistant Rag1-/- mice. Monoclonal Ab B4 was found to specifically recognize mouse annexin IV. Pre-injection of recombinant annexin IV blocked IR injury in wild type C57BL/6 mice, demonstrating the requirement for recognition of this protein in order to develop IR injury in the context of a complex natural antibody repertoire. Humans were also found to exhibit IgM natural antibodies that recognize annexin IV. These data in toto identify annexin IV as a key ischemia-related target antigen that is recognized by natural Abs in a pathologic process required in vivo to develop intestinal IR injury."
GSE14870_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14871_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14872_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14873_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14874_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14876_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14877_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14890_series_matrix.txtimp_info.txt
TRIF r is 3 
Found -/- in !Series_title	"Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice."
GSE14890_series_matrix.txtimp_info.txt
TRIF r is 3 
Found -/- in !Series_overall_design	"Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."
GSE14890_series_matrix.txtimp_info.txt
TRIF r is 5 
Found stimulated in !Series_overall_design	"Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."
GSE14891_series_matrix.txtimp_info.txt
Zc3h12a r is 1 
Found -/- in !Series_title	"Expression data of LPS-stimulated macrophages from wild-type and Zc3h12a-/- mice."
GSE14891_series_matrix.txtimp_info.txt
Zc3h12a r is 1 
Found -/- in !Series_overall_design	"Peritoneal macrophages from wild-type and Zc3h12a-/- mice were stimulated with LPS for 0, 1, 2 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."
GSE14891_series_matrix.txtimp_info.txt
Zc3h12a r is 6 
Found stimulated in !Series_title	"Expression data of LPS-stimulated macrophages from wild-type and Zc3h12a-/- mice."
GSE14891_series_matrix.txtimp_info.txt
Zc3h12a r is 5 
Found stimulated in !Series_overall_design	"Peritoneal macrophages from wild-type and Zc3h12a-/- mice were stimulated with LPS for 0, 1, 2 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed."
GSE14892_series_matrix.txtimp_info.txt
Spdef r is 1 
Found -/- in !Series_overall_design	"To compare wild-type versus Spdef-/- intestinal or colonic tissue samples, pooled total RNA from 2-3 littermates were utilized for each experiment. In addition, tissue samples from both adult (P30) or E18.5 fetal mice were compared. Overall, we carried out 3 dye swap experiments for E18.5 small intestine and P30 colon resulting in 6 arrays each, and 2 dye swap experiments for E18.5 colon and P30 small intestine resulting in 4 arrays each."
GSE14898_series_matrix.txtimp_info.txt
Tie2 r is 5 
Found expressing in !Series_summary	"Methods: Beginning at 8 weeks of age, male Tie2-GFP mice (transgenically expressing green fluorescent protein exclusively within the endothelia) were fed a 60% fat calorie diet (Bio-Serv #S3282); age-matched mice were fed normal chow. After 4, 6, and 8 weeks on the diet, aortae and skeletal muscles (gastrocnemius, biceps femoris, and plantaris) were excised, minced, and collagenolytically digested. Each tissue digest was then subjected to FACS in order to obtain 10,000 endothelial cells. Transcriptomic analyses were performed with microarrays containing the Operon Murine V4 oligo set, and highly dysregulated genes were confirmed by real-time PCR. Results: By 4 weeks, Tie2-GFP mice receiving a high fat diet exhibited a fasting glucose of 215+17 mg/dL vs. 134+23 mg/dL in controls; by 6 weeks, a high fat diet resulted in lower glucose tolerance vs. control diet. Following 4, 6, and 8 weeks of high-fat regimen, aortic endothelial transcripts up-regulated by greater than 2-fold in biologically replicate experiments included macrophage inflammatory protein 2 (Mip2), chemokine (C-C motif) ligand 9 (CCL9), galectin-3 (Gal-3), and 5-lipoxygenase-activating protein (FLAP). Endothelial transcripts up-regulated in skeletal muscle included Mip2, CCL8 and 9, FLAP, gal-1 and 3, and ferritin light chain 1 (FTL1); transcripts down-regulated in muscle included endothelin-1 (ET-1) and insulin-like growth factor II (IGF II). Discussion: Gal-3 and FTL-1 are known to increase in response to advanced glycation end-products and oxidized LDL, respectively. However, the down-regulation of ET-1 and IGFII was surprising, as the transcription of these genes has previously been thought to exacerbate atherosclerosis. In conclusion, a comprehensive analysis of the endothelial transcript-level response to a dietary model of Type II diabetes has revealed novel regulation of transcripts with roles in inflammation, insulin sensitivity, oxidative stress, and atherosclerosis. Understanding the mechanism of diabetes-associated endothelial dysfunction may lead to improved therapies that lower the risk of cardiovascular complications in diabetic patients. "
GSE14906_series_matrix.txtimp_info.txt
FOG2 r is 1 
Found null in !Series_overall_design	"We have analyzed 6 RNA samples total (3 from control hearts, 2 from FOG2 null hearts and 1 from GATA4ki hearts)"
GSE14907_series_matrix.txtimp_info.txt
Eda r is 1 
Found mutant in !Series_summary	"Sweat glands play a fundamental role in thermal regulation in man, but the molecular mechanism of their development remains unknown. To initiate analyses, we compared the model of Eda mutant Tabby mice, in which sweat glands were not formed, to wild-type mice.  We inferred developmental stages and critical genes based on observations at 7 time points spanning embryonic, postnatal and adult life. In wild-type footpads, sweat gland germs were detected at E17.5. The coiling of secretory portions started at postnatal day 1 (P1), and sweat gland formation was essentially complete by P5. Consistent with a controlled morphological progression, expression profiling revealed stage-specific gene expression changes. Similar to the development of hair follicles     the other major skin appendage controlled by EDA     sweat gland induction and initial progression was accompanied by Eda-dependent up-regulation of the Shh pathway. During the further development of sweat gland secretory portions, Foxa1 and Foxi1, not at all expressed in hair follicles, were progressively up-regulated in wild-type but not in Tabby footpads. Upon completion of wild-type development, Shh declined to Tabby levels, but Fox family genes remained at elevated levels in mature sweat glands. The results provide a framework for the further analysis of phased downstream regulation of gene action, possibly by a signaling cascade, in response to Eda."
GSE14917_series_matrix.txtimp_info.txt
Cebpa r is 3 
Found deletion in !Series_summary	"We have previously demonstrated that deletion of the Cebpa gene in the developing fetal mouse lung caused death soon after birth from the failure of lung maturation.  Many of the transcriptional pathways regulating morphogenesis of the fetal lung are induced postnatally and mediate repair of the injured lung.  We hypothesized that C/EBPa plays a role in protection of the alveolar epithelium following hyperoxia injury of the mature lung.  Transgenic Cebpa∆/∆ mice in which Cebpa was conditionally deleted from Clara cells (from early gestation) and type II cells (from near-term) were developed.  Cebpa∆/∆ mice grow normally without any pulmonary abnormalities. Cebpa∆/∆ mice were highly susceptible to hyperoxia. Cebpa∆/∆ mice died within 4d after hyperoxia associated with severe lung inflammation and altered surfactant components at a time when all control mice survived.  Microarrays were analyzed on isolated type II cells at an early stage (24h) of hyperoxia exposure to detect the primary genes influenced by deletion of Cebpa.  The associated network analysis revealed the reduced expression of key genes related to surfactant lipid and protein homeostasis, such as Srebf, Scap, Lpcat1, Abca3, Sftpb, and Napsa.  Genes for the cell signaling, immune response, and protective antioxidants, including GSH and Vnn-1,3, were decreased in the Cebpa∆/∆ mice lung.  C/EBPa did not play a critical role in postnatal pulmonary function under normal conditions.  In contrast, in the absence of C/EBPa, exposure to hyperoxia caused respiratory failure, supporting the concept that C/EBPa plays an important role in enhancing epithelial cell survival, surfactant lipid homeostasis, and maturation of SP-B from pro-SP-B. "
GSE14920_series_matrix.txtimp_info.txt
PPARalpha r is 1 
Found deficient in !Series_overall_design	"One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array"
GSE14920_series_matrix.txtimp_info.txt
Ctrl r is 4 
Found treated in !Series_overall_design	"One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array"
GSE14920_series_matrix.txtimp_info.txt
PPARalpha r is 7 
Found treated in !Series_overall_design	"One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array"
GSE14921_series_matrix.txtimp_info.txt
PPAR-alpha r is 5 
Found deletion in !Series_summary	"Hepatic metabolic derangements are key components in the development of fatty liver, insulin resistance, and atherosclerosis. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Here we demonstrate that hepatic SIRT1 regulates fatty acid metabolism by positively regulating PPAR-alpha. Hepatocyte-specific deletion of SIRT1 impairs PPAR-alpha signaling and decreased fatty acid beta-oxidation in the liver. When challenged with a high-fat diet, liver-specific SIRT1 knockout mice develop hepatic steatosis, hepatic inflammation, and endoplasmic reticulum stress. Taken together, our data indicate that SIRT1 plays a vital role in the regulation of hepatic lipid homeostasis."
GSE14921_series_matrix.txtimp_info.txt
Lox r is 7 
Found KO in !Series_overall_design	"ix Lox control and six Liver-specific SIRT1 KO (SIRT1 LKO) mice in 95% C57BL/6 background were fed ad libitum with free access to water and food. They were then sacrificed at 4:00pm to analyze PPAR-alpha mediated phenotypes under physiologically relevant conditions. Livers from these mice were then dissected and RNA was isolated with a Qiagen RNA easy mini kit with on-column DNAseI treatment. RNA quality was validated with the Agilent 2100 Bioanalyzer in the microarray facility. RNA samples were then pooled with 2 animals/replicate and analyzed by Agilent Whole Mouse arrays. Data are generated by the Rosetta Resolver Error Model."
GSE14929_series_matrix.txtimp_info.txt
Ppara r is 1 
Found -/- in !Series_title	"Myocardial expression data from gnotobiotic wild-type and Ppara-/- mice"
GSE14929_series_matrix.txtimp_info.txt
Ppara r is 1 
Found -/- in !Series_summary	"Germ free (GF) and conventionalized (CONV-D) wild-type C57Bl/6 male mice in the CARB-fed, 24h fasted, and 30d trained states; plus GF and CONV-D CARB-fed Ppara-/- mice.  CARB-fed indicates a standard polysaccharide-rich mouse chow diet."
GSE14929_series_matrix.txtimp_info.txt
Ppara r is 1 
Found -/- in !Series_overall_design	"Hearts from six to ten week-old GF and CONV-D mice, from the following eight treatment groups (GF, CONV-D) X (CARB-fed [wild-type], 24h fast [wild-type], 30d trained [wild-type], Ppara-/- [CARB-fed])"
GSE14969_series_matrix.txtimp_info.txt
TNF-alpha r is 1 
Found induced in !Series_summary	"Although natural antibodies (NAbs) are present from birth, little is known about what drives their selection, and whether they have housekeeping functions. We now show that the prototypic T15-NAb, first identified because of its protective role in infection, is representative of a previously unknown type of NAb response that specifically recognizes and forms complexes with apoptotic cells, and which promotes cell-corpse engulfment by phagocytes. This T15-NAb-mediated process is dependent on the recruitment of C1q and mannose-binding lectin (MBL), which have known immune modulatory activities that also provide “eat me” signals for phagocytic clearance. Further investigation revealed that, the addition of T15-NAb significantly suppressed in vitro macrophage LPS-induced TNF-alpha and IL-6 secretion, as well as in vitro Toll-like receptor (TLR)-induced dendritic cell maturation and secretion of pro-inflammatory cytokines and chemokines. Significantly, high doses of this B-1 cell produced NAb also inhibited in vivo TLR–induced pro-inflammatory responses, and could suppress autoimmune inflammatory arthritis. These studies identify and characterize a previously unknown regulatory circuit by which a NAb product of innate-like B cells aids homeostasis by control of fundamental inflammatory pathways."
GSE14971_series_matrix.txtimp_info.txt
Cux2 r is 1 
Found knock-out in !Series_title	"Comparative gene expression profile of Cux2 knock-out cortex"
GSE14971_series_matrix.txtimp_info.txt
Cux2 r is 1 
Found ko in !Series_summary	"Gene expression profiles of Cux2 ko cortex was compared to the profile of WT cortex."
GSE14971_series_matrix.txtimp_info.txt
Cux2 r is 1 
Found ko in !Series_overall_design	"Cerebral cortex of WT and Cux2 ko animals were dissected and total RNA was obtained. Gene expression profiles were obtained for each sample and compared."
GSE14980_series_matrix.txtimp_info.txt
Gata1 r is 8 
Found deficient in !Series_summary	"G1ME cells are GATA1-deficient murine bipotential megakaryocyte/erythrocyte progenitor cells derived from Gata1-negative murine ES cells.  In order to assess the impact of GATA1 on gene regulation and cell differentiation, an expression construct was used to transiently produce high levels of GATA1.  Cells transduced with this construct or a vector control were harvested at 18 and 42 hours, and gene expression was analyzed using Affymetrix MOE430 version 2 arrays."
GSE14984_series_matrix.txtimp_info.txt
P5 r is 2 
Found deletion in !Series_overall_design	"Comparison 1: wild type vs. PWS deletion in P5 non-starved mice;"
GSE14984_series_matrix.txtimp_info.txt
P5 r is 2 
Found deletion in !Series_overall_design	"Comparison 2: wild type vs. PWS deletion in P5 fasting mice;"
GSE14984_series_matrix.txtimp_info.txt
P5 r is 2 
Found deletion in !Series_overall_design	"Comparison 4: non-starved vs. fasting in P5 PWS deletion mice;"
GSE10341_series_matrix.txtimp_info.txt
Th r is 4 
Found deficient in !Series_summary	"The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown.  When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at E13.5-E14.5, they resemble wild type fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage and edema. At E12.5, prior to the appearance of morphological deficits associated with Th deletion, catecholamine-deficient fetuses are preferentially killed by experimentally-induced hypoxia and have lower tissue pO2 than wild type siblings.  Catecholamine-deficient fetuses also induced HIF-1 target genes to a greater extent than wild type siblings, supporting the notion that null fetuses experience greater hypoxia or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby, improving oxygen delivery in wild type mice. Surprisingly, increasing maternal oxygen (FiO2 33% or 63%) prevents the effects of catecholamine-deficiency, restoring heart rate, myocardial mass and survival of Th null fetuses.  We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis as vulnerability to constitutive hypoxia increases as fetal growth accelerates during normal development."
GSE10341_series_matrix.txtimp_info.txt
Th r is 4 
Found deficient in !Series_summary	"The catecholamine norepinephrine is required for fetal survival, but its essential function is unknown.  When catecholamine-deficient [tyrosine hydroxylase (Th) null] mouse fetuses die at E13.5-E14.5, they resemble wild type fetuses exposed to hypoxia. They exhibit bradycardia (28% reduction in heart rate), thin ventricular myocardium (20% reduction in tissue), epicardial detachment, and death with vascular congestion, hemorrhage and edema. At E12.5, prior to the appearance of morphological deficits associated with Th deletion, catecholamine-deficient fetuses are preferentially killed by experimentally-induced hypoxia and have lower tissue pO2 than wild type siblings.  Catecholamine-deficient fetuses also induced HIF-1 target genes to a greater extent than wild type siblings, supporting the notion that null fetuses experience greater hypoxia or have an enhanced response to hypoxia. Hypoxia induces a 13-fold increase in plasma norepinephrine levels, which would be expected to increase heart rate, thereby, improving oxygen delivery in wild type mice. Surprisingly, increasing maternal oxygen (FiO2 33% or 63%) prevents the effects of catecholamine-deficiency, restoring heart rate, myocardial mass and survival of Th null fetuses.  We suggest that norepinephrine mediates fetal survival by maintaining oxygen homeostasis as vulnerability to constitutive hypoxia increases as fetal growth accelerates during normal development."
GSE10341_series_matrix.txtimp_info.txt
Th r is 1 
Found -/- in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
Th r is 1 
Found -/- in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
tyrosine hydroxylase r is 5 
Found -/- in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
Th r is 2 
Found null in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
Th r is 2 
Found null in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
tyrosine hydroxylase r is 2 
Found null in !Series_overall_design	"The first aim was to compare gene expression of E12.5 mouse fetuses between wild type (Th+/+) versus tyrosine hydroxylase null (Th-/-) animals from normoxic dams. This resulted in 6 arrays."
GSE10341_series_matrix.txtimp_info.txt
tyrosine hydroxylase r is 2 
Found null in !Series_overall_design	"The second aim compared wild type and tyrosine hydroxylase null E12.5 fetuses from dam exposed to hypoxia (8% oxygen) for 6 hours prior to sacrifice at E12.5 of gestation. This resulted in 6 arrays."
GSE10421_series_matrix.txtimp_info.txt
Smad4 r is 3 
Found deficient in !Series_summary	"Results: Among 1419 transcripts significantly modulated by the dietary iron content, four were regulated similarly to the hepcidin genes Hamp1 and Hamp2. They are coding for Bmp6, the regulator of Bmp/Smad signal transduction Smad7, the negative regulator of basic helix-loop-helix (bHLH) proteins Id1, and a protein with a bHLH domain, Atoh8. The iron overload developed by Smad4 and Hamp1-deficient mice also increased Bmp6 transcription. Body iron stores influence Smad1/5/8 phosphorylation and, as shown by analysis of mice with liver-specific disruption of Smad4, the binding partner for the receptor-activated Smads is necessary for activation of Smad7, Id1, and Atoh8 transcription by iron."
GSE10421_series_matrix.txtimp_info.txt
hepcidin r is 6 
Found induced in !Series_summary	"Background & Aims: Although hepcidin expression was shown to be induced by the BMP signaling pathway, it is not yet known how iron regulates hepcidin and which of the BMP molecules is the endogenous regulator of iron homeostasis in vivo. We therefore assessed liver transcription profiles of mice fed an iron-deficient or an iron-enriched diet and looked for genes that were regulated similarly to hepcidin in that context."
GSE13493_series_matrix.txtimp_info.txt
Rag2 r is 1 
Found deficient in !Series_title	"Expression data from developing thymocytes of N15TCR transgenic Rag2 deficient mice"
GSE13493_series_matrix.txtimp_info.txt
TCR r is 3 
Found deficient in !Series_summary	"We used microarrays to identify the genes differentially expressed during CD8 single positive T cell development in N15 TCR transgenic Rag2 deficient mice."
GSE13493_series_matrix.txtimp_info.txt
Rag2 r is 1 
Found deficient in !Series_summary	"We used microarrays to identify the genes differentially expressed during CD8 single positive T cell development in N15 TCR transgenic Rag2 deficient mice."
GSE13493_series_matrix.txtimp_info.txt
TCR r is 4 
Found -/- in !Series_overall_design	"We have analyzed gene expression in the individual populations as development proceeds from DP, intermediate (Int), to SP subsets. To this end, we sorted the individual populations from six age and sex matched 5-6 week old N15 TCR tg+/+ RAG-2-/- H-2b mice for two independent experiments. For sorting subpopulations, cells were stained with anti-CD4 (L3T4) and anti-CD8 (Ly-2) antibodies (Pharmingen, San Diego, CA USA) and DP, Int and SP thymocytes were sorted on a MoFlo (Cytomation, Fort Collins, CO USA)."