new figures from pmc; updated config and log

figure_fetch.log

@@ -706,3 +706,25 @@
 
 2024-10-02 07:18:04 - ==========================================================
 
+2024-10-03 02:18:59 - Starting NCBI PMC Figure Fetcher
+
+2024-10-03 02:18:59 - Configuration loaded from query_config.yml
+
+2024-10-03 02:18:59 - PMC search query: (((((((((((signaling pathway[Figure/Table Caption]) OR signalling pathway[Figure/Table Caption]) OR regulatory pathway[Figure/Table Caption]) OR disease pathway[Figure/Table Caption]) OR drug pathway[Figure/Table Caption]) OR metabolic pathway[Figure/Table Caption]) OR biosynthetic pathway[Figure/Table Caption]) OR synthesis pathway[Figure/Table Caption]) OR cancer pathway[Figure/Table Caption]) OR response pathway[Figure/Table Caption]) OR cycle pathway[Figure/Table Caption])) AND (2024/07/01[PUBDATE] : 2024/08/01[PUBDATE])
+
+2024-10-03 02:19:34 - PMC search completed. Fetched 1066 results (max set to 3000).
+
+2024-10-03 02:19:43 - Extracted 1535 figures from XML content.
+
+2024-10-03 02:19:43 - Identified 461 pathway figures.
+
+2024-10-03 02:19:43 - Skipped 448 figures previously processed.
+
+2024-10-03 02:19:43 - Processed 13 pathway figures for download.
+
+2024-10-03 02:19:55 - New pathway figures downloaded: 13
+
+2024-10-03 02:19:55 - NCBI PMC Figure Fetcher completed
+
+2024-10-03 02:19:55 - ==========================================================
+

figures/PMC11379071__ijbsv20p4146g003.yml

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+---
+figid: PMC11379071__ijbsv20p4146g003
+pmcid: PMC11379071
+image_filename: ijbsv20p4146g003.jpg
+figure_link: /pmc/articles/PMC11379071/figure/F3/
+number: Figure 3
+figure_title: LATS2 mediates the reduction in GSH levels by targeting PSAT1 in HB
+  cells.
+caption: LATS2 mediates the reduction in GSH levels by targeting PSAT1 in HB cells.
+  (A-C) HepG2 and HUH6 cells were transfected with LATS2. YAP1 was simultaneously
+  overexpressed, and ferroptosis-related metabolic parameters, including the GSH concentration
+  (A), phospholipid level (B), and iron concentration (C), were measured. (D-F) The
+  relative levels of glycine (D), cysteine (E), and glutamine were measured under
+  the indicated conditions. (G) Transcriptional levels of the key enzymes of the serine
+  synthesis pathway were screened by qRT‒PCR after LATS2 overexpression, with or without
+  YAP1 overexpression. (H) The expression of LATS2, YAP1, and PSAT1 was measured by
+  WB under the indicated conditions. (I) CCK-8 assays were conducted after LATS2 overexpression,
+  with or without PSAT1 overexpression. (J and K) Lipid ROS levels were measured by
+  C11-Bodipy staining coupled with flow cytometry under the indicated treatments.
+  All quantitative data are shown as the mean ± SD from three independent experiments.
+  n.s., no significant difference, *p <0.05, **p <0.01, ***p <0.001, ****p <0.0001
+article_title: N6-methyladenosine modification of LATS2 promotes hepatoblastoma progression
+  by inhibiting ferroptosis through the YAP1/ATF4/PSAT1 axis
+citation: Guoqing Zhu, et al. Int J Biol Sci. 2024;20(11).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-8-1
+doi: 10.7150/ijbs.92413
+journal_title: International Journal of Biological Sciences
+journal_nlm_ta: Int J Biol Sci
+publisher_name: Ivyspring International Publisher
+keywords:
+- hepatoblastoma
+- ferroptosis
+- LATS2
+- Hippo/YAP
+- m6A methylation
+---

figures/PMC11379071__ijbsv20p4146g004.yml

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+---
+figid: PMC11379071__ijbsv20p4146g004
+pmcid: PMC11379071
+image_filename: ijbsv20p4146g004.jpg
+figure_link: /pmc/articles/PMC11379071/figure/F4/
+number: Figure 4
+figure_title: LATS2 stimulates PSAT1 transcription via the YAP/ATF4 pathway.
+caption: LATS2 stimulates PSAT1 transcription via the YAP/ATF4 pathway. (A and B)
+  The promoter of PSAT1 was mutated as indicated (A), and luciferase activity was
+  measured using a dual-luciferase system after the indicated vectors were transfected
+  into HepG2 and HUH6 cells (B). (C) The PSAT1 promoter activity of wild-type (WT)
+  and mutant (Del-1) strains was measured using a dual-luciferase system in HepG2
+  and HUH6 cells with simultaneous overexpression of LATS2, with or without YAP1.
+  (D and E) Chromatin was immunoprecipitated using an anti-YAP1 antibody or negative
+  control anti-IgG antibody (D), and qRT-PCR (E) was then conducted on HepG2 and HUH6
+  cells. (F) Predicted binding site (PBS) of YAP1 and the promoter of PSAT1 according
+  to bioinformatics analysis of GSE99315. (G) Reciprocal co-IP of YAP1 and ATF4 was
+  performed using anti-YAP1 and anti-ATF4 antibodies, respectively, followed by WB
+  using the indicated antibodies in HepG2 and HUH6 cells. (H) Colocalization of YAP1
+  and ATF4 in HepG2 and HUH6 cells, as measured by confocal microscopy. Scale bar,
+  50 μm. (I and J) Chromatin was immunoprecipitated using an anti-ATF4 antibody or
+  negative control anti-IgG antibody (I), and qPCR (J) was then conducted in HepG2
+  and HUH6 cells. (K) The PSAT1 promoter activity of the WT and Del-1 strains was
+  measured using a dual-luciferase system in HepG2 and HUH6 cells with simultaneous
+  overexpression of PSAT1. (L and M) The protein (L) and mRNA (M) expression levels
+  of PSAT1 were measured under the indicated treatments. (N-P) Ferroptotic events
+  in YAP1-overexpressing cells with or without ATF4 knockdown were evaluated by measuring
+  cell viability (N), lipid ROS levels (O), and MDA production (P). (Q) The relative
+  level of cysteine was detected under the indicated conditions. All quantitative
+  data are shown as the mean ± SD from three independent experiments. **p <0.01, ***p
+  <0.001, ****p <0.0001
+article_title: N6-methyladenosine modification of LATS2 promotes hepatoblastoma progression
+  by inhibiting ferroptosis through the YAP1/ATF4/PSAT1 axis
+citation: Guoqing Zhu, et al. Int J Biol Sci. 2024;20(11).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-8-1
+doi: 10.7150/ijbs.92413
+journal_title: International Journal of Biological Sciences
+journal_nlm_ta: Int J Biol Sci
+publisher_name: Ivyspring International Publisher
+keywords:
+- hepatoblastoma
+- ferroptosis
+- LATS2
+- Hippo/YAP
+- m6A methylation
+---

figures/PMC11379071__ijbsv20p4146g005.yml

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+---
+figid: PMC11379071__ijbsv20p4146g005
+pmcid: PMC11379071
+image_filename: ijbsv20p4146g005.jpg
+figure_link: /pmc/articles/PMC11379071/figure/F5/
+number: Figure 5
+figure_title: METTL3 mediates LATS2 mRNA instability and expression via m6A modification.
+caption: METTL3 mediates LATS2 mRNA instability and expression via m6A modification.
+  (A) Corresponding KEGG pathways were identified according to the significant genes
+  with upregulated m6A methylation. (B) The relative m6A enrichment levels of the
+  LATS2 mRNA 5′UTR were verified via meRIP-qPCR analysis in HepG2 and HUH6 cells.
+  (C-E) The mRNA expression of LATS2 (C), the protein expression of METTL3, YAP1,
+  p-YAP1, and LATS2 (D), and the relative m6A enrichment of LATS2 (E) were measured
+  with or without METTL3 knockdown. (F-H) The mRNA expression of LATS2 (F), the protein
+  expression of METTL3, YAP1, p-YAP1, and LATS2 (G), and the relative m6A enrichment
+  of LATS2 (H) were measured in cells with or without METTL3 overexpression. (I and
+  J) The decay rate of LATS2 mRNA was detected via qRT-PCR at the indicated time points
+  after METTL3 knockdown (I) or overexpression (J) in HUH6 and HepG2 cells treated
+  with ActD (5 μg/ml). (K) The m6A levels of the WT and Mut pmir-GlO plasmids were
+  verified by MeRIP-qPCR. (L and M) Luciferase activities of the WT and Mut pmir-GlO
+  plasmids were measured after METTL3 knockdown (L) or overexpression (M) in HepG2
+  and HUH6 cells. All quantitative data are presented as the mean ± SD from three
+  independent experiments. WT, wild-type; Mut, mutation; n.s., no significant difference;
+  **p <0.01, ***p <0.001, ****p <0.0001
+article_title: N6-methyladenosine modification of LATS2 promotes hepatoblastoma progression
+  by inhibiting ferroptosis through the YAP1/ATF4/PSAT1 axis
+citation: Guoqing Zhu, et al. Int J Biol Sci. 2024;20(11).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-8-1
+doi: 10.7150/ijbs.92413
+journal_title: International Journal of Biological Sciences
+journal_nlm_ta: Int J Biol Sci
+publisher_name: Ivyspring International Publisher
+keywords:
+- hepatoblastoma
+- ferroptosis
+- LATS2
+- Hippo/YAP
+- m6A methylation
+---

figures/PMC11379071__ijbsv20p4146g008.yml

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+---
+figid: PMC11379071__ijbsv20p4146g008
+pmcid: PMC11379071
+image_filename: ijbsv20p4146g008.jpg
+figure_link: /pmc/articles/PMC11379071/figure/F8/
+number: Figure 8
+figure_title: A diagram illustrating the underlying molecular mechanism identified
+  in the present study.
+caption: A diagram illustrating the underlying molecular mechanism identified in the
+  present study. Mechanistically, increased m6A modification of the LATS2 mRNA, which
+  is recognized by YTHDF2, facilitates its degradation through the CCR4-NOT complex.
+  Reduced LATS2 expression activates YAP1, promoting GSH synthesis via the ATF4/PSAT1
+  pathway, ultimately enhancing ferroptosis resistance
+article_title: N6-methyladenosine modification of LATS2 promotes hepatoblastoma progression
+  by inhibiting ferroptosis through the YAP1/ATF4/PSAT1 axis
+citation: Guoqing Zhu, et al. Int J Biol Sci. 2024;20(11).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-8-1
+doi: 10.7150/ijbs.92413
+journal_title: International Journal of Biological Sciences
+journal_nlm_ta: Int J Biol Sci
+publisher_name: Ivyspring International Publisher
+keywords:
+- hepatoblastoma
+- ferroptosis
+- LATS2
+- Hippo/YAP
+- m6A methylation
+---

figures/PMC11379076__ijbsv20p4178g002.yml

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+---
+figid: PMC11379076__ijbsv20p4178g002
+pmcid: PMC11379076
+image_filename: ijbsv20p4178g002.jpg
+figure_link: /pmc/articles/PMC11379076/figure/F2/
+number: Figure 2
+figure_title: The mTORC1/2 signaling pathways.
+caption: The mTORC1/2 signaling pathways. The receptor tyrosine kinases (RTKs)/PI3K/Akt
+  signaling pathway, stimulated by growth factors, is pivotal to mTOR protein regulation.
+  PI3K, typically maintained at a basal level, is activated to synthesize phosphatidylinositol
+  3,4,5-triphosphate (PIP3) from phosphatidylinositol 4,5-bisphosphate (PIP2). This
+  process is counteracted by the tumor suppressor PTEN. PIP2 and PIP3 trigger AKT
+  phosphorylation, leading to TSC2 inactivation and Rheb-GTP generation. Upon phosphorylation
+  by mTORC1, ULK1/2 induces autophagy by phosphorylating Beclin-1
+article_title: 'mTOR Signaling: Roles in Hepatitis B Virus Infection and Hepatocellular
+  Carcinoma'
+citation: Ling Mei, et al. Int J Biol Sci. 2024;20(11).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-8-1
+doi: 10.7150/ijbs.95894
+journal_title: International Journal of Biological Sciences
+journal_nlm_ta: Int J Biol Sci
+publisher_name: Ivyspring International Publisher
+keywords:
+- mammalian target of rapamycin
+- hepatitis B virus
+- hepatocellular carcinoma
+- mTOR inhibitors
+---

figures/PMC11379076__ijbsv20p4178g003.yml

@@ -0,0 +1,29 @@
+---
+figid: PMC11379076__ijbsv20p4178g003
+pmcid: PMC11379076
+image_filename: ijbsv20p4178g003.jpg
+figure_link: /pmc/articles/PMC11379076/figure/F3/
+number: Figure 3
+figure_title: The Interaction between mTOR pathway and HCC.
+caption: The Interaction between mTOR pathway and HCC. HBx activates the PI3K/AKT/mTOR
+  signaling pathway by increasing the expression of AFP and activating IKKβ, which
+  encourages malignant transformation. Besides, the accumulation of mutant L-HBsAg
+  and excessive L-HBsAg could also activate the mTOR signaling pathway. Then the activated
+  mTOR promotes carcinogenic-related life activities, such as aerobic glycolysis,
+  angiogenesis, lipogenesis, migration, inflammation, and cell cycle
+article_title: 'mTOR Signaling: Roles in Hepatitis B Virus Infection and Hepatocellular
+  Carcinoma'
+citation: Ling Mei, et al. Int J Biol Sci. 2024;20(11).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-8-1
+doi: 10.7150/ijbs.95894
+journal_title: International Journal of Biological Sciences
+journal_nlm_ta: Int J Biol Sci
+publisher_name: Ivyspring International Publisher
+keywords:
+- mammalian target of rapamycin
+- hepatitis B virus
+- hepatocellular carcinoma
+- mTOR inhibitors
+---

figures/PMC11383372__jciinsight-9-173240-g044.yml

@@ -0,0 +1,36 @@
+---
+figid: PMC11383372__jciinsight-9-173240-g044
+pmcid: PMC11383372
+image_filename: jciinsight-9-173240-g044.jpg
+figure_link: /pmc/articles/PMC11383372/figure/F4/
+number: Figure 4
+figure_title: MIF downregulates adipose LPL expression through a CXCR/Akt signaling
+  pathway
+caption: '(A–C) Recombinant mouse MIF protein (400 ng/mL) was incubated with differentiated
+  3T3-L1 adipocytes for 24 hours, and LPL expression and activity were measured. Mature
+  adipocytes were initially isolated from WT and Cd74–/– mice, and suspended cells
+  were treated with vehicle or recombinant mouse MIF (rMIF, 400 ng/mL) for 24 hours.
+  (D) Lpl gene was quantified by qPCR. In 3T3-L1 adipocytes, rMIF was incubated with
+  the CXCR2 or CXCR4 inhibitors, SB225002 (400nM) and WZ811 (5μM). (E and F) The levels
+  of Lpl gene and proteins and Akt phosphorylation were subsequently evaluated. (G)
+  MIF regulated Akt phosphorylation and LPL protein expression in the presence of
+  insulin were assessed by Western blot. All data are analyzed by Student’s t test
+  or 1-way ANOVA and presented as mean ± SD. *P ≤ 0.05 increase vs. rMIF group in
+  E, vs. other groups in G; #P ≤ 0.05 reduction vs. vehicle in A–D and G, vs. other
+  groups in E and F, vs. insulin in G'
+article_title: Downregulation of adipose LPL by PAR2 contributes to the development
+  of hypertriglyceridemia
+citation: Yiheng Huang, et al. JCI Insight. 2024 Jul 8;9(13).
+year: '2024'
+pub_date: 2024-7-8
+epub_date: 2024-7-8
+doi: 10.1172/jci.insight.173240
+journal_title: JCI Insight
+journal_nlm_ta: JCI Insight
+publisher_name: American Society for Clinical Investigation
+keywords:
+- Metabolism
+- Adipose tissue
+- Cytokines
+- Signal transduction
+---

figures/PMC11402474__nihms-2019520-f0006.yml

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+---
+figid: PMC11402474__nihms-2019520-f0006
+pmcid: PMC11402474
+image_filename: nihms-2019520-f0006.jpg
+figure_link: /pmc/articles/PMC11402474/figure/F5/
+number: Figure 5.
+figure_title: Cardiac CRTC KD and OE concertedly regulate metabolism in the heart
+caption: (A) Venn diagram showing up- and downregulated genes in response to cardiac-specific
+  KD or OE of CRTC. Bolded numbers in the center represent genes that are concertedly
+  regulated by CRTC; 106 are DOWN with CRTC OE and UP with CRTC KD, 34 are UP with
+  CRTC OE and DOWN with CRTC KD.(B) Significantly affected GO categories for the 140
+  concertedly regulated genes are primarily pathways involved in metabolic regulation.
+  (“Count” indicates the number of genes affected in the GO category).(C) Whole-body
+  triglyceride levels were significantly reduced in CRTC systemic mutant flies (left)
+  and were also significantly reduced in cardiac-specific CRTC-KD flies (right). Ctrl1
+  flies were w1118 and Crtl2 flies were tinCD4-Ga4/+. (Plots show all data points,
+  max, min, median, and p values; significance by unpaired t test [left] and one-way
+  ANOVA with Tukey’s multiple comparisons post hoc test [right])
+article_title: The nutrient sensor CRTC and Sarcalumenin/thinman represent an alternate
+  pathway in cardiac hypertrophy
+citation: Cristiana Dondi, et al. Cell Rep. 2024 Sep 11;43(8).
+year: '2024'
+pub_date: 2024-9-11
+epub_date: 2024-8-01
+doi: 10.1016/j.celrep.2024.114549
+journal_title: Cell reports
+journal_nlm_ta: Cell Rep
+publisher_name: .na.character
+keywords: []
+---

figures/PMC11402474__nihms-2019520-f0008.yml

@@ -0,0 +1,29 @@
+---
+figid: PMC11402474__nihms-2019520-f0008
+pmcid: PMC11402474
+image_filename: nihms-2019520-f0008.jpg
+figure_link: /pmc/articles/PMC11402474/figure/F7/
+number: Figure 7.
+figure_title: CRTC affects cardiac function in hiPSC-cardiomyocytes
+caption: (A) Representative voltage traces from control siRNA- and siCRTC-transfected
+  cardiomyocytes. APs were recorded optically from individual cardiomyocytes. APD
+  at 75% of repolarization (APD75) was significantly increased with siRNA-mediated
+  KD of CRTC2 and CRTC3. (Plots show max, min, median, and p values; siCtrl n = 1,338,
+  siCRTC1 n = 1,459, siCRTC2 n = 1,427, siCRTC3 n = 1,326; significance by one-way
+  ANOVA with Tukey’s multiple comparisons post hoc test).(B) RT-qPCR quantification
+  showing reduction in SRL expression in iPSC-CMs after siRNA CRTC KD. (Significance
+  by one-way ANOVA with Tukey’s multiple comparisons post hoc test).(C) siRNA KD of
+  SRL prolongs APD75 in hiPSC-CMs (unpaired t test).(D) Model of proposed CaN-CRTC-SRL
+  signaling pathway
+article_title: The nutrient sensor CRTC and Sarcalumenin/thinman represent an alternate
+  pathway in cardiac hypertrophy
+citation: Cristiana Dondi, et al. Cell Rep. 2024 Sep 11;43(8).
+year: '2024'
+pub_date: 2024-9-11
+epub_date: 2024-8-01
+doi: 10.1016/j.celrep.2024.114549
+journal_title: Cell reports
+journal_nlm_ta: Cell Rep
+publisher_name: .na.character
+keywords: []
+---

figures/PMC11405054__jci-134-174598-g215.yml

@@ -0,0 +1,35 @@
+---
+figid: PMC11405054__jci-134-174598-g215
+pmcid: PMC11405054
+image_filename: jci-134-174598-g215.jpg
+figure_link: /pmc/articles/PMC11405054/figure/F1/
+number: Figure 1
+figure_title: Fibroblasts from ILD biopsies have higher TGF-β signaling than fibroblasts
+  from ILD explants
+caption: (A) Schematic of processing diagnostic lung biopsies of ILD patients. (B)
+  Dimensional reduction plot of fibroblasts from donor (13,856 cells, n = 13), ILD
+  biopsy (7,724 cells, n = 3), and IPF explant (21,192 cells, n = 26) samples. (C)
+  Fibroblast subtype composition by sample type. (D and E) Volcano plots of differentially
+  expressed (D.E.) genes in all fibroblasts from ILD biopsy samples versus donor samples
+  and ILD biopsy samples versus IPF explant samples, with selected TGF-β pathway–related
+  genes labeled. (F) Violin plot of selected TGF-β1–related genes in all fibroblasts.
+  (G) Single-cell activity of hallmark TGF-β pathway in all fibroblasts. (H) Heatmap
+  of z scores from pairwise upstream IPA of differentially expressed genes from all
+  fibroblasts. Statistical significance was determined by 2-tailed t test (C, F, and
+  G) and MAST with adjustment for multiple comparisons (D and E)
+article_title: A fibroblast-dependent TGF-β1/sFRP2 noncanonical Wnt signaling axis
+  promotes epithelial metaplasia in idiopathic pulmonary fibrosis
+citation: Max L. Cohen, et al. J Clin Invest. 2024 Jul 9;134(18).
+year: '2024'
+pub_date: 2024-7-9
+epub_date: 2024-7-9
+doi: 10.1172/JCI174598
+journal_title: The Journal of Clinical Investigation
+journal_nlm_ta: J Clin Invest
+publisher_name: American Society for Clinical Investigation
+keywords:
+- Pulmonology
+- Cytokines
+- Fibrosis
+- Human stem cells
+---