mypub_articles.bib

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@ARTICLE{Haft2013,
  author = {Haft D. H. and Selengut J. D. and Richter R. A. and
	Harkins D. and \textbf{Basu M. K.} and Beck E.},
  title = {{TIGRFAMs} and Genome Properties in 2013.},
  journal = {Nucleic Acids Res},
  year = {2013},
  volume = {41},
  pages = {D387--D395},
  number = {D1},
  month = {Jan},
  abstract = {TIGRFAMs, available online at http://www.jcvi.org/tigrfams is a database
	of protein family definitions. Each entry features a seed alignment
	of trusted representative sequences, a hidden Markov model (HMM)
	built from that alignment, cutoff scores that let automated annotation
	pipelines decide which proteins are members, and annotations for
	transfer onto member proteins. Most TIGRFAMs models are designated
	equivalog, meaning they assign a specific name to proteins conserved
	in function from a common ancestral sequence. Models describing more
	functionally heterogeneous families are designated subfamily or domain,
	and assign less specific but more widely applicable annotations.
	The Genome Properties database, available at http://www.jcvi.org/genome-properties,
	specifies how computed evidence, including TIGRFAMs HMM results,
	should be used to judge whether an enzymatic pathway, a protein complex
	or another type of molecular subsystem is encoded in a genome. TIGRFAMs
	and Genome Properties content are developed in concert because subsystems
	reconstruction for large numbers of genomes guides selection of seed
	alignment sequences and cutoff values during protein family construction.
	Both databases specialize heavily in bacterial and archaeal subsystems.
	At present, 4284 models appear in TIGRFAMs, while 628 systems are
	described by Genome Properties. Content derives both from subsystem
	discovery work and from biocuration of the scientific literature.},
  doi = {10.1093/nar/gks1234},
  institution = {Informatics, J Craig Venter Institute, Rockville, MD 20850 and Informatics,
	J Craig Venter Institute, La Jolla, CA 92121, USA.},
  language = {eng},
  medline-pst = {ppublish},
  owner = {malay},
  pii = {gks1234},
  pmid = {23197656},
  note = {{PMID:} 23197656},
  timestamp = {2013.01.18},
  url = {http://dx.doi.org/10.1093/nar/gks1234}
}

@article{basu_prophylo:_2011,
	title = {{ProPhylo:} Partial Phylogenetic Profiling to guide protein family construction and assignment of biological process},
	volume = {12},
	issn = {1471-2105},
	shorttitle = {{ProPhylo}},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/22070167},
	doi = {10.1186/1471-2105-12-434},
	abstract = {{ABSTRACT:}  {BACKGROUND:} Phylogenetic profiling is a technique of scoring co-occurrence between a protein family and some other trait, usually another protein family, across a set of taxonomic groups. In spite of several refinements in recent years, the technique still invites significant improvement. To be its most effective, a phylogenetic profiling algorithm must be able to examine co-occurrences among protein families whose boundaries are uncertain within large homologous protein superfamilies. {RESULTS:} Partial Phylogenetic Profiling {(PPP)} is an iterative algorithm that scores a given taxonomic profile against the taxonomic distribution of families for all proteins in a genome. The method works through optimizing the boundary of each protein family, rather than by relying on prebuilt protein families or fixed sequence similarity thresholds. Double Partial Phylogenetic Profiling {(DPPP)} is a related procedure that begins with a single sequence and searches for optimal granularities for its surrounding protein family in order to generate the best query profiles for {PPP.}  We present {ProPhylo}, a high-performance software package for phylogenetic profiling studies through creating individually optimized protein family boundaries. {ProPhylo} provides precomputed databases for immediate use and tools for manipulating the taxonomic profiles used as queries.  {CONCLUSION:} {ProPhylo} results show universal markers of methanogenesis, a new {DNA} phosphorothioation-dependent restriction enzyme, and efficacy in guiding protein family construction. The software and the associated databases are freely available under the open source Perl Artistic License from ftp://ftp.jcvi.org/pub/data/ppp/.},
	number = {1},
	journal = {{BMC} Bioinform},
	author = {\textbf{$^*$Basu M. K.} and Selengut J. D. and $^*$Haft D. H.},
	month = nov,
	year = {2011},
	note = {{PMID:} 22070167},
	pages = {434}
}

@ARTICLE{,
  author = {{Daphnia Genome Consortium}},
  title = {{T}he ecoresponsive genome of \emph{{D}aphnia pulex}.},
  journal = {Science},
  year = {2011},
  volume = {331},
  pages = {555--561},
  number = {6017},
  month = {Feb},
  abstract = {We describe the draft genome of the microcrustacean Daphnia pulex,
	which is only 200 megabases and contains at least 30,907 genes. The
	high gene count is a consequence of an elevated rate of gene duplication
	resulting in tandem gene clusters. More than a third of Daphnia's
	genes have no detectable homologs in any other available proteome,
	and the most amplified gene families are specific to the Daphnia
	lineage. The coexpansion of gene families interacting within metabolic
	pathways suggests that the maintenance of duplicated genes is not
	random, and the analysis of gene expression under different environmental
	conditions reveals that numerous paralogs acquire divergent expression
	patterns soon after duplication. Daphnia-specific genes, including
	many additional loci within sequenced regions that are otherwise
	devoid of annotations, are the most responsive genes to ecological
	challenges.},
  doi = {10.1126/science.1197761},
  institution = {Center for Genomics and Bioinformatics, Indiana University, 915 East
	Third Street, Bloomington, IN 47405, USA. jcolbour@indiana.edu},
  language = {eng},
  medline-pst = {ppublish},
  owner = {mbasu},
  pii = {331/6017/555},
  pmid = {21292972},
  timestamp = {2011.02.18},
  url = {http://dx.doi.org/10.1126/science.1197761}
}


@article{haft_biological_2011,
	title = {Biological systems discovery in silico: radical {S-adenosylmethionine} protein families and their target peptides for posttranslational modification},
	volume = {193},
	issn = {1098-5530},
	shorttitle = {Biological systems discovery in silico},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/21478363},
	doi = {10.1128/JB.00040-11},
	abstract = {Data mining methods in bioinformatics and comparative genomics commonly rely on working definitions of protein families from prior computation. Partial phylogenetic profiling {(PPP)}, by contrast, optimizes family sizes during its searches for the cooccurring protein families that serve different roles in the same biological system. In a large-scale investigation of the incredibly diverse radical S-adenosylmethionine {(SAM)} enzyme superfamily, {PPP} aided in building a collection of 68 {TIGRFAMs} hidden Markov models {(HMMs)} that define nonoverlapping and functionally distinct subfamilies. Many identify radical {SAM} enzymes as molecular markers for multicomponent biological systems; {HMMs} defining their partner proteins also were constructed. Newly found systems include five groupings of protein families in which at least one marker is a radical {SAM} enzyme while another, encoded by an adjacent gene, is a short peptide predicted to be its substrate for posttranslational modification. The most prevalent, in over 125 genomes, featuring a peptide that we designate {SCIFF} (six cysteines in forty-five residues), is conserved throughout the class Clostridia, a distribution inconsistent with putative bacteriocin activity. A second novel system features a tandem pair of putative peptide-modifying radical {SAM} enzymes associated with a highly divergent family of peptides in which the only clearly conserved feature is a run of {His-Xaa-Ser} repeats. A third system pairs a radical {SAM} domain peptide maturase with selenocysteine-containing targets, suggesting a new biological role for selenium. These and several additional novel maturases that cooccur with predicted target peptides share a C-terminal additional {4Fe4S-binding} domain with {PqqE}, the subtilosin A maturase {AlbA}, and the predicted mycofactocin and Nif11-class peptide maturases as well as with activators of anaerobic sulfatases and quinohemoprotein amine dehydrogenases. Radical {SAM} enzymes with this additional domain, as detected by {TIGR04085}, significantly outnumber lantibiotic synthases and cyclodehydratases combined in reference genomes while being highly enriched for members whose apparent targets are small peptides. Interpretation of comparative genomics evidence suggests unexpected (nonbacteriocin) roles for natural products from several of these systems.},
	number = {11},
	journal = {J. Bacteriol.},
	author = {Haft D. H. and \textbf{Basu M. K.}},
	month = jun,
	year = {2011},
	note = {{PMID:} 21478363},
	keywords = {Bacterial Proteins, Computational Biology, Protein Processing, {Post-Translational}, {S-Adenosylmethionine}},
	pages = {2745--2755}
}



@article{Basu2010_expansion,
	title = {Expansion of ribosomally produced natural products: a nitrile hydratase- and Nif11-related precursor family},
	volume = {8},
	issn = {1741-7007},
	shorttitle = {Expansion of ribosomally produced natural products},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/20500830},
	doi = {10.1186/1741-7007-8-70},
	abstract = {{BACKGROUND:} A new family of natural products has been described in which cysteine, serine and threonine from ribosomally-produced peptides are converted to thiazoles, oxazoles and methyloxazoles, respectively. These metabolites and their biosynthetic gene clusters are now referred to as thiazole/oxazole-modified microcins {(TOMM).} As exemplified by microcin B17 and streptolysin S, {TOMM} precursors contain an N-terminal leader sequence and C-terminal core peptide. The leader sequence contains binding sites for the posttranslational modifying enzymes which subsequently act upon the core peptide. {TOMM} peptides are small and highly variable, frequently missed by gene-finders and occasionally situated far from the thiazole/oxazole forming genes. Thus, locating a substrate for a particular {TOMM} pathway can be a challenging endeavor. {RESULTS:} Examination of candidate {TOMM} precursors has revealed a subclass with an uncharacteristically long leader sequence closely related to the enzyme nitrile hydratase. Members of this nitrile hydratase leader peptide {(NHLP)} family lack the metal-binding residues required for catalysis. Instead, {NHLP} sequences display the classic {Gly-Gly} cleavage motif and have C-terminal regions rich in heterocyclizable residues. The {NHLP} family exhibits a correlated species distribution and local clustering with an {ABC} transport system. This study also provides evidence that a separate family, annotated as Nif11 nitrogen-fixing proteins, can serve as natural product precursors {(N11P),} but not always of the {TOMM} variety. Indeed, a number of cyanobacterial genomes show extensive {N11P} paralogous expansion, such as Nostoc, Prochlorococcus and Cyanothece, which replace the {TOMM} cluster with lanthionine biosynthetic machinery. {CONCLUSIONS:} This study has united numerous {TOMM} gene clusters with their cognate substrates. These results suggest that two large protein families, the nitrile hydratases and Nif11, have been retailored for secondary metabolism. Precursors for {TOMMs} and lanthionine-containing peptides derived from larger proteins to which other functions are attributed, may be widespread. The functions of these natural products have yet to be elucidated, but it is probable that some will display valuable industrial or medical activities.},
	journal = {{BMC} Biology},
	author = {Haft D. H. and  \textbf{Basu M. K.} and Mitchell D. A.},
	year = {2010},
	note = {{PMID:} 20500830},
	keywords = {My publication},
	pages = {70}
}
@article{Rogozin2009_analysis_of_rare,
    abstract = {The deep phylogeny of eukaryotes is an important but extremely difficult problem of evolutionary biology. Five eukaryotic supergroups are relatively well established but the relationship between these supergroups remains elusive, and their divergence seems to best fit a "Big Bang" model. Attempts were made to root the tree of eukaryotes by using potential derived shared characters such as unique fusions of conserved genes. One popular model of eukaryotic evolution that emerged from this type of analysis is the unikont-bikont phylogeny: The unikont branch consists of Metazoa, Choanozoa, Fungi, and Amoebozoa, whereas bikonts include the rest of eukaryotes, namely, Plantae (green plants, Chlorophyta, and Rhodophyta), Chromalveolata, excavates, and Rhizaria. We reexamine the relationships between the eukaryotic supergroups using a genome-wide analysis of rare genomic changes (RGCs) associated with multiple, conserved amino acids (RGC\_CAMs and RGC\_CAs), to resolve trifurcations of major eukaryotic lineages. The results do not support the basal position of Chromalveolata with respect to Plantae and unikonts or the monophyly of the bikont group and appear to be best compatible with the monophyly of unikonts and Chromalveolata. Chromalveolata show a distinct, additional signal of affinity with Plantae, conceivably, owing to genes transferred from the secondary, red algal symbiont. Excavates are derived forms, with extremely long branches that complicate phylogenetic inference; nevertheless, the RGC analysis suggests that they are significantly more likely to cluster with the unikont-Chromalveolata assemblage than with the Plantae. Thus, the first split in eukaryotic evolution might lie between photosynthetic and nonphotosynthetic forms and so could have been triggered by the endosymbiosis between an ancestral unicellular eukaryote and a cyanobacterium that gave rise to the chloroplast. 10.1093/gbe/evp011},
    author = {Rogozin I. B. and \textbf{Basu, M. K.} and Csürös M. and Koonin E. V.},
    journal = {Genome Biol Evol},
    month = {June},
    number = {0},
    pages = {99--113},
    posted-at = {2009-09-18 01:40:28},
    priority = {2},
    title = {Analysis of Rare Genomic Changes Does Not Support the Unikont-Bikont Phylogeny and Suggests Cyanobacterial Symbiosis as the Point of Primary Radiation of Eukaryotes},
    volume = {2009},
    year = {2009},
note={{PMID:} 20333181}
}

@ARTICLE{Basu2008d,
  author = {\textbf{Basu M. K.} and Rogozin I. B. and Koonin E. V.},
  title = {Primordial spliceosomal introns were probably {U}2-type},
  journal = {Trends Genet},
  year = {2008},
  volume= {24},
  number= {11},
  pages={525-8},
  owner = {mbasu},
  note={PMID:18824272},
  timestamp = {2008.03.21}
}


@ARTICLE{Basu2008c,
  author = {\textbf{Basu M. K.} and Makalowski W. and Rogozin I. B. and Koonin E. V.},
  title = {{U}12 intron positions are more strongly conserved between animals
	and plants than {U}2 intron positions},
  journal = {Biol Direct},
  year = {2008},
  volume={3},
  number={1},
  pages={19},
  owner = {mbasu},
  note= {PMID: 18479526},
  timestamp = {2008.03.21}
}

@ARTICLE{Basu2008b,
  author = {\textbf{Basu M. K.} and Carmel L. and Rogozin I. B. and Koonin E. V.},
  title = {{E}volution of protein domain promiscuity in eukaryotes},
  journal = {Genome Res.},
  year = {2008},
  volume = {18},
  pages = {449-61},
  number = {3},
  note = {PMID: 18230802}
}



@ARTICLE{Basu2008a,
  author = {\textbf{Basu M. K.} and Rogozin I. B. and Deusch O. and Dagan T.
	and Martin W. and Koonin E. V.},
  title = {{E}volutionary dynamics of introns in plastid-derived genes in plants:
	saturation nearly reached but slow intron gain continues},
  journal = {Mol Biol Evol},
  year = {2008},
  volume = {25},
  pages = {111-9},
  note = {PMID: 17974547},
  abstract = {Some of the principal transitions in the evolution of eukaryotes are
	characterized by engulfment of prokaryotes by primitive eukaryotic
	cells. In particular, approximately 1.6 billion years ago, engulfment
	of a cyanobacterium that became the ancestor of chloroplasts and
	other plastids gave rise to Plantae, the major branch of eukaryotes
	comprised of glaucophytes, red algae, green algae, and green plants.
	After endosymbiosis, there was large-scale migration of genes from
	the endosymbiont to the nuclear genome of the host such that approximately
	18\% of the nuclear genes in Arabidopsis appear to be of chloroplast
	origin. To gain insights into the process of evolution of gene structure
	in these, originally, intronless genes, we compared the properties
	and the evolutionary dynamics of introns in genes of plastid origin
	and ancestral eukaryotic genes in Arabidopsis, poplar, and rice genomes.
	We found that intron densities in plastid-derived genes were slightly
	but significantly lower than those in ancestral eukaryotic genes.
	Although most of the introns in both categories of genes were conserved
	between monocots (rice) and dicots (Arabidopsis and poplar), lineage-specific
	intron gain was more pronounced in plastid-derived genes than in
	ancestral genes, whereas there was no significant difference in the
	intron loss rates between the 2 classes of genes. Thus, after the
	transfer to the nuclear genome, the plastid-derived genes have undergone
	a massive intron invasion that, by the time of the divergence of
	dicots and monocots (150-200 MYA), yielded intron densities only
	slightly lower than those in ancestral genes. Nevertheless, the accumulation
	of introns in plastid-derived genes appears not to have reached saturation
	and continues to this time, albeit at a low rate. The overall pattern
	of intron gain and loss in the plastid-derived genes is shaped by
	this continuing gain and the more general tendency for loss that
	is characteristic of the recent evolution of plant genes.},
  issn = {07374038}
}

@ARTICLE{Babenko2006,
  author = {Babenko V. N. and \textbf{Basu M. K.} and Kondrashov F. A. and Rogozin I. B. and Koonin E. V.},
  title = {{S}igns of positive selection of somatic mutations in human cancers
	detected by {EST} sequence analysis},
  journal = {BMC cancer},
  year = {2006},
  volume = {6},
  pages = {36},
  note = {PMID: 16469093},
  abstract = {BACKGROUND: Carcinogenesis typically involves multiple somatic mutations
	in caretaker (DNA repair) and gatekeeper (tumor suppressors and oncogenes)
	genes. Analysis of mutation spectra of the tumor suppressor that
	is most commonly mutated in human cancers, p53, unexpectedly suggested
	that somatic evolution of the p53 gene during tumorigenesis is dominated
	by positive selection for gain of function. This conclusion is supported
	by accumulating experimental evidence of evolution of new functions
	of p53 in tumors. These findings prompted a genome-wide analysis
	of possible positive selection during tumor evolution. METHODS: A
	comprehensive analysis of probable somatic mutations in the sequences
	of Expressed Sequence Tags (ESTs) from malignant tumors and normal
	tissues was performed in order to access the prevalence of positive
	selection in cancer evolution. For each EST, the numbers of synonymous
	and non-synonymous substitutions were calculated. In order to identify
	genes with a signature of positive selection in cancers, these numbers
	were compared to: i) expected numbers and ii) the numbers for the
	respective genes in the ESTs from normal tissues. RESULTS: We identified
	112 genes with a signature of positive selection in cancers, i.e.,
	a significantly elevated ratio of non-synonymous to synonymous substitutions,
	in tumors as compared to 37 such genes in an approximately equal-sized
	EST collection from normal tissues. A substantial fraction of the
	tumor-specific positive-selection candidates have experimentally
	demonstrated or strongly predicted links to cancer. CONCLUSION: The
	results of EST analysis should be interpreted with extreme caution
	given the noise introduced by sequencing errors and undetected polymorphisms.
	Furthermore, an inherent limitation of EST analysis is that multiple
	mutations amenable to statistical analysis can be detected only in
	relatively highly expressed genes. Nevertheless, the present results
	suggest that positive selection might affect a substantial number
	of genes during tumorigenic somatic evolution.},
  issn = {14712407},
  keywords = {Amino Acid Sequence,Amino Acid Substitution,Evolution, Molecular,Expressed
	Sequence Tags,Genes, Neoplasm,Humans,Molecular Sequence Data,Mutation,Neoplasms,Polymorphism,
	Single Nucleotide,Sequence Alignment,Sequence Analysis, Protein}
}

@ARTICLE{Basu2005,
  author = {\textbf{Basu M. K.} and Koonin E. V.},
  title = {{E}volution of eukaryotic cysteine sulfinic acid reductase, sulfiredoxin
	({S}rx), from bacterial chromosome partitioning protein {P}ar{B}},
  journal = {Cell cycle},
  year = {2005},
  volume = {4},
  pages = {947-52},
  month = jul,
  note = {PMID: 15917647},
  abstract = {Sufiredoxin (Srx) is a sulfinic acid reductase, a recently identified
	eukaryotic enzyme, which is involved in the reduction of the hyperoxidized
	sulfinic acid form of the catalytic cysteine of 2-Cys peroxiredoxins
	(Prx). This reaction contributes to the oxidative stress response
	and H2O2 mediated signaling. We show that Srx has significant sequence
	and structural similarity to a functionally unrelated protein, ParB,
	a DNA-binding protein with a helix-turn-helix (HTH) domain which
	is involved in chromosome partitioning in bacteria. Sequence comparison
	and phylogenetic analysis of the Srx and ParB protein families suggest
	that Srx evolved via truncation of ParB, which removed the entire
	C-terminal half of the protein, including the HTH domain, and a substitution
	of cysteine for a glutamic acid in a highly conserved structural
	motif of ParB. The latter substitution apparently created the sulfinic
	acid reductase catalytic site. Evolution of a redox enzyme from a
	DNA-binding protein, with retention of highly significant sequence
	similarity, is unusual, even when compared to functional switches
	accompanying recruitment of other prokaryotic proteins for new functions
	in eukaryotes.},
  issn = {15514005},
  keywords = {Amino Acid Sequence,Bacterial Proteins,Chromosome Segregation,Chromosomes,
	Bacterial,Cysteine,Evolution, Molecular,Molecular Sequence Data,Oxidoreductases,Oxidoreductases
	Acting on Sulfur Group Donors,Phylogeny,Saccharomyces cerevisiae
	Proteins,Sequence Homology, Amino Acid}
}

@ARTICLE{Rogozin2005,
  author = {Rogozin I. B. and \textbf{Basu M. K} and Jordan I. K. and Pavlov Y. I.
	and Koonin E. V.},
  title = {{APOBEC}4, a new member of the {AID}/{APOBEC} family of polynucleotide
	(deoxy)cytidine deaminases predicted by computational analysis},
  journal = {Cell cycle},
  year = {2005},
  volume = {4},
  pages = {1281-5},
  month = sep,
  note = {PMID: 16082223},
  abstract = {Using iterative database searches, we identified a new subfamily of
	the AID/APOBEC family of RNA/DNA editing cytidine deaminases. The
	new subfamily, which is represented by readily identifiable orthologs
	in mammals, chicken, and frog, but not fishes, was designated APOBEC4.
	The zinc-coordinating motifs involved in catalysis and the secondary
	structure of the APOBEC4 deaminase domain are evolutionarily conserved,
	suggesting that APOBEC4 proteins are active polynucleotide (deoxy)cytidine
	deaminases. In reconstructed maximum likelihood phylogenetic trees,
	APOBEC4 forms a distinct clade with a high statistical support. APOBEC4
	and APOBEC1 are joined in a moderately supported cluster clearly
	separated from AID, APOBEC2 and APOBEC3 subfamilies. In mammals,
	APOBEC4 is expressed primarily in testis which suggests the possibility
	that it is an editing enzyme for mRNAs involved in spermatogenesis.},
  issn = {15514005},
  keywords = {Amino Acid Motifs,Amino Acid Sequence,Animals,Cluster Analysis,Computational
	Biology,Cytidine Deaminase,Cytosine Deaminase,Escherichia coli,Evolution,
	Molecular,Humans,Likelihood Functions,Male,Mice,Models, Statistical,Molecular
	Sequence Data,Nucleoside Deaminases,Phylogeny,Protein Conformation,RNA
	Editing,RNA, Messenger,Software,Tissue Distribution,Xenopus,Zinc}
}

@ARTICLE{Basu2001,
  author = {\textbf{$^*$Basu M. K.}},
  title = {{S}e{W}e{R}: a customizable and integrated dynamic {HTML} interface
	to bioinformatics services},
  journal = {Bioinformatics},
  year = {2001},
  volume = {17},
  pages = {577-8},
  month = jun,
  note = {PMID: 11395442},
  abstract = {SUMMARY: Sequence analysis using Web Resources (SeWeR) is an integrated,
	Dynamic HTML (DHTML) interface to commonly used bioinformatics services
	available on the World Wide Web. It is highly customizable, extendable,
	platform neutral, completely server-independent and can be hosted
	as a web page as well as being used as stand-alone software running
	within a web browser.},
  issn = {13674803},
  keywords = {Computational Biology,Database Management Systems,Hypermedia,Information
	Services,Information Storage and Retrieval,Internet,User-Computer
	Interface}
}

@ARTICLE{Ray1998,
  author = {Ray M. K. and Kumar G. S. and Janiyani K. and Kannan K. and Jagtap
	P. and \textbf{Basu M. K.} and Shivaji S.},
  title = {{A}daptation to low temperature and regulation of gene expression
	in {A}ntarctic psychrotrophic bacteria},
  journal = {J Biosci},
  year = {1998},
  volume = {23},
  pages = {423--35},
  number = {4},
  owner = {mbasu},
  timestamp = {2008.01.11}
}

@ARTICLE{Basu2009,
  author = {\textbf{$^*$Basu M. K.} and Poliakov E. and Rogozin I. B.},
  title = {Domain mobility in proteins: functional and evolutionary implications},
  journal = {Brief Bioinform.},
  year = {2009},
  owner = {mbasu},
  note={PMID:19151098},
  timestamp = {2008.03.21},
  volume = {10},
  number = {3},
  pages = {205-16}
}


@article{yu2019,
  title = {Grammar of Protein Domain Architectures},
  author = {Yu L. and Tanwar D. K. and Penha E. D. S. and Wolf Y. I. and Koonin E. V. and \textbf{$^*$Basu M. K.}},
  year = {2019},
  volume = {116},
  pages = {3636--3645},
  issn = {0027-8424, 1091-6490},
  doi = {10.1073/pnas.1814684116},
  abstract = {From an abstract, informational perspective, protein domains appear analogous to words in natural languages in which the rules of word association are dictated by linguistic rules, or grammar. Such rules exist for protein domains as well, because only a small fraction of all possible domain combinations is viable in evolution. We employ a popular linguistic technique, n-gram analysis, to probe the ``proteome grammar''\textemdash that is, the rules of association of domains that generate various domain architectures of proteins. Comparison of the complexity measures of ``protein languages'' in major branches of life shows that the relative entropy difference (information gain) between the observed domain architectures and random domain combinations is highly conserved in evolution and is close to being a universal constant, at {$\sim$}1.2 bits. Substantial deviations from this constant are observed in only two major groups of organisms: a subset of Archaea that appears to be cells simplified to the limit, and animals that display extreme complexity. We also identify the n-grams that represent signatures of the major branches of cellular life. The results of this analysis bolster the analogy between genomes and natural language and show that a ``quasi-universal grammar'' underlies the evolution of domain architectures in all divisions of cellular life. The nearly universal value of information gain by the domain architectures could reflect the minimum complexity of signal processing that is required to maintain a functioning cell.},
  copyright = {Copyright \textcopyright{} 2019 the Author(s). Published by PNAS.. This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).},
  file = {/Users/malay/local/zotero_data/storage/3G2P5885/yu2019-grammar_of_protein_domain_architectures.pdf},
  journal = {Proc Natl Acad Sci U S A},
  language = {en},
  number = {9},
  note = {PMID: 30733291}
}

@article{jin2020,
  title = {{{STRAP}} Regulates Alternative Splicing Fidelity during Lineage Commitment of Mouse Embryonic Stem Cells},
  author = {Jin L. and Chen Y. and Crossman D. K. and Datta A. and Vu T. and Mobley J. A. and \textbf{Basu M. K.} and Scarduzio M. and Wang H. and Chang C. and Datta P. K.},
  year = {2020},
  volume = {11},
  pages = {5941},
  issn = {2041-1723},
  doi = {10.1038/s41467-020-19698-6},
  abstract = {Alternative splicing (AS) is involved in cell fate decisions and embryonic development. However, regulation of these processes is poorly understood. Here, we have identified the serine threonine kinase receptor-associated protein (STRAP) as a putative spliceosome-associated factor. Upon Strap deletion, there are numerous AS events observed in mouse embryoid bodies (EBs) undergoing a neuroectoderm-like state. Global mapping of STRAP-RNA binding in mouse embryos by enhanced-CLIP sequencing (eCLIP-seq) reveals that STRAP preferably targets transcripts for nervous system development and regulates AS through preferred binding positions, as demonstrated for two neuronal-specific genes, Nnat and Mark3. We have found that STRAP involves in the assembly of 17S U2 snRNP proteins. Moreover, in Xenopus, loss of Strap leads to impeded lineage differentiation in embryos, delayed neural tube closure, and altered exon skipping. Collectively, our findings reveal a previously unknown function of STRAP in mediating the splicing networks of lineage commitment, alteration of which may be involved in early embryonic lethality in mice.},
  file = {/Users/malay/local/zotero_data/storage/LH4YD8I3/jin2020-strap_regulates_alternative_splicing_fidelity_during_lineage_commitment_of.pdf},
  journal = {Nat Commun},
  language = {eng},
  number = {1},
  pmcid = {PMC7684319},
  note = {PMID: 33230114}
}

@article{basu2020,
  title = {Exome {{Sequencing Identifies Abnormalities}} in {{Glycosylation}} and {{ANKRD36C}} in {{Patients}} with {{Immune}}-{{Mediated Thrombotic Thrombocytopenic Purpura}}},
  author = {\textbf{$^*$Basu M. K.} and Massicano F. and Yu L. and Halkidis K. and Pillai V. and Cao W. and Zheng L. and {$^*$Zheng X. L.}},
  year = {2020},
  month = nov,
  issn = {2567-689X},
  doi = {10.1055/s-0040-1719030},
  abstract = {BACKGROUND: Immune-mediated thrombotic thrombocytopenic purpura (iTTP) is a potentially fatal blood disorder, resulting from autoantibodies against ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13). However, the mechanism underlying anti-ADAMTS13 autoantibody formation is not known, nor it is known how genetic aberrations contribute to the pathogenesis of iTTP. METHODS: Here we performed whole exome sequencing (WES) of DNA samples from 40 adult patients with iTTP and 15 local healthy subjects with no history of iTTP and other hematological disorders. RESULTS: WES revealed variations in the genes involved in protein glycosylation, including O-linked glycosylation, to be a major pathway affected in patients with iTTP. Moreover, variations in the ANKRD gene family, particularly ANKRD36C and its paralogs, were also more prevalent in patients with iTTP than in the healthy controls. The ANKRD36 family of proteins have been implicated in inflammation. Mass spectrometry revealed a dramatic alternation in plasma glycoprotein profile in patients with iTTP compared with the healthy controls. CONCLUSION: Altered glycosylation may affect the disease onset and progression in various ways: it may predispose patients to produce ADAMTS13 autoantibodies or affect their binding properties; it may also alter clearance kinetics of hemostatic and inflammatory proteins. Together, our findings provide novel insights into plausible mechanisms underlying the pathogenesis of iTTP.},
  journal = {Thromb Haemost},
  language = {eng},
  note = {PMID: 33184803}
}

@article{spurlock2019,
  title = {New Quantitative Approach Reveals Heterogeneity in Mitochondrial Structure-Function Relations in Tumor-Initiating Cells},
  author = {Spurlock B. and Gupta P. and \textbf{Basu M. K.} and Mukherjee A. and Hjelmeland A. B. and {Darley-Usmar} V. and Parker D. and Foxall M. E. and Mitra K.},
  year = {2019},
  month = may,
  volume = {132},
  issn = {1477-9137},
  doi = {10.1242/jcs.230755},
  abstract = {Steady-state mitochondrial structure or morphology is primarily maintained by a balance of opposing fission and fusion events between individual mitochondria, which is collectively referred to as mitochondrial dynamics. The details of the bidirectional relationship between the status of mitochondrial dynamics (structure) and energetics (function) require methods to integrate these mitochondrial aspects. To study the quantitative relationship between the status of mitochondrial dynamics (fission, fusion, matrix continuity and diameter) and energetics (ATP and redox), we have developed an analytical approach called mito-SinCe2 After validating and providing proof of principle, we applied mito-SinCe2 on ovarian tumor-initiating cells (ovTICs). Mito-SinCe2 analyses led to the hypothesis that mitochondria-dependent ovTICs interconvert between three states, that have distinct relationships between mitochondrial energetics and dynamics. Interestingly, fusion and ATP increase linearly with each other only once a certain level of fusion is attained. Moreover, mitochondrial dynamics status changes linearly with ATP or with redox, but not simultaneously with both. Furthermore, mito-SinCe2 analyses can potentially predict new quantitative features of the opposing fission versus fusion relationship and classify cells into functional classes based on their mito-SinCe2 states.This article has an associated First Person interview with the first author of the paper.},
  file = {/Users/malay/local/zotero_data/storage/QG84A55V/spurlock2019-new_quantitative_approach_reveals_heterogeneity_in_mitochondrial.pdf},
  journal = {J Cell Sci},
  language = {eng},
  number = {9},
  pmcid = {PMC6526706},
  note = {PMID: 30910831}
}

@article{ping2017,
  title = {Mutations in {Coagulation Factor VIII} are associated with more favorable outcome in Patients with Cutaneous Melanoma},
  author = {Ping Z. and Soni A. and Williams L. A. and Pham H. P. and \textbf{Basu M. K.} and Zheng. X. L.},
  year = {2017},
  month = jul,
  volume = {1},
  pages = {e113-e121},
  issn = {2512-9465},
  doi = {10.1055/s-0037-1607337},
  abstract = {Coagulation factor VIII (FVIII), von Willebrand factor (VWF), and ADAMTS13 play an important role in regulation of normal hemostasis. However, little is known about their roles in patients with malignancy, particularly with cutaneous melanoma. Whole genome sequencing data are available for 25,719 cases in 126 cancer genomic studies for analysis. All sequencing data and corresponding pathology findings were obtained from The Cancer Genome Atlas. The cBioportal bioinformatics tools were used for the data analysis. Our results demonstrated that mutations in genes encoding FVIII, VWF, and ADAMTS13 were reported in 92 of 126 cancer genomic studies and high mutation rates in these three genes were observed in patients with cutaneous melanoma from three independent studies. Moreover, high mutation rates in FVIII, VWF, and ADAMTS13 were also found in patients with diffuse large B cell lymphoma (22.9\%), lung small cell carcinoma (20.7\%), and colon adenocarcinoma (19.4\%). Among 366 melanoma cases from TCGA provisional, the somatic mutation rates of FVIII, VWF and ADAMTS13 in tumor cells were 15\%, 14\%, and 5\%, respectively. There was a strong tendency for coexisting mutations of FVIII, VWF, and ADAMTS13. Kaplan-Meier survival analysis demonstrated that melanoma patients with FVIII mutations had a more favorable overall survival rate than those without FVIII mutations (p=0.02). These findings suggest for the first time that the FVIII mutation burden may have a prognostic value for patients with cutaneous melanoma. Further studies are warranted to delineate the molecular mechanisms underlying the favorable prognosis associated with FVIII mutations.},
  file = {/Users/malay/local/zotero_data/storage/CLX6GF8I/ping2017-mutations_in_coagulation_factor_viii_are_associated_with_more_favorable_outcome.pdf},
  journal = {TH Open},
  language = {eng},
  number = {2},
  pmcid = {PMC5690574},
  note = {PMID: 29152610}
}
@article{tanwar2016,
  title = {Crosstalk between the Mitochondrial Fission Protein, {{Drp1}}, and the Cell Cycle Is Identified across Various Cancer Types and Can Impact Survival of Epithelial Ovarian Cancer Patients},
  author = {Tanwar D. K. and Parker D. J. and Gupta P. and Spurlock B. and Alvarez R. D. and \textbf{$^*$Basu M. K.} and Mitra K.},
  year = {2016},
  month = aug,
  issn = {1949-2553},
  doi = {10.18632/oncotarget.11047},
  abstract = {Mitochondrial metabolic reprogramming is a hallmark of tumorigenesis. Although mitochondrial function can impact cell cycle regulation it has been an understudied area in cancer research. Our study highlights a specific involvement of mitochondria in cell cycle regulation across cancer types. The mitochondrial fission process, which is regulated at the core by Drp1, impacts various cellular functions. Drp1 has been implicated in various cancer types with no common mechanism reported. Our Drp1-directed large-scale analyses of the publically available cancer genomes reveal a robust correlation of Drp1 with cell-cycle genes in 29 of the 31 cancer types examined. Hypothesis driven investigation on epithelial ovarian cancer (EOC) revealed that Drp1 co-expresses specifically with the cell-cycle module responsible for mitotic transition. Repression of Drp1 in EOC cells can specifically attenuate mitotic transition, establishing a potential casual role of Drp1 in mitotic transition. Interestingly, Drp1-Cell-Cycle co-expression module is specifically detected in primary epithelial ovarian tumors that robustly responded to chemotherapy, suggesting that Drp1 driven mitosis may underlie chemo-sensitivity of the primary tumors. Analyses of matched primary and relapsed EOC samples revealed a Drp1-based-gene-expression-signature that could identify patients with poor survival probabilities from their primary tumors. Our results imply that around 60\% of platinum-sensitive EOC patients undergoing relapse show poor survival, potentially due to further activation of a mitochondria driven cell-cycle regime in their recurrent disease. We speculate that this patient group could possibly benefit from mitochondria directed therapies that are being currently evaluated at various levels, thus enabling targeted or personalized therapy based cancer management.},
  file = {/Users/malay/local/zotero_data/storage/2V9BKS2T/Tanwar2016_Crosstalk between the mitochondrial fission protein, Drp1, and the cell cycle.pdf},
  journal = {Oncotarget},
  language = {ENG},
  note = {PMID: 27509055}
}

@article{parker2015,
  title = {A New Mitochondrial Pool of Cyclin {{E}}, Regulated by {{Drp1}}, Is Linked to Cell-Density-Dependent Cell Proliferation},
  author = {Parker D. J. and Iyer A. and Shah S. and Moran A. and Hjelmeland A. B. and \textbf{Basu M. K.} and Liu R. and Mitra K.},
  year = {2015},
  month = nov,
  volume = {128},
  pages = {4171--4182},
  issn = {1477-9137},
  doi = {10.1242/jcs.172429},
  abstract = {The regulation and function of the crucial cell cycle regulator cyclin E (CycE) remains elusive. Unlike other cyclins, CycE can be uniquely controlled by mitochondrial energetics, the exact mechanism being unclear. Using mammalian cells (in vitro) and Drosophila (in vivo) model systems in parallel, we show that CycE can be directly regulated by mitochondria through its recruitment to the organelle. Active mitochondrial bioenergetics maintains a distinct mitochondrial pool of CycE (mtCycE) lacking a key phosphorylation required for its degradation. Loss of the mitochondrial fission protein dynamin-related protein 1 (Drp1, SwissProt O00429 in humans) augments mitochondrial respiration and elevates the mtCycE pool allowing CycE deregulation, cell cycle alterations and enrichment of stem cell markers. Such CycE deregulation after Drp1 loss attenuates cell proliferation in low-cell-density environments. However, in high-cell-density environments, elevated MEK-ERK signaling in the absence of Drp1 releases mtCycE to support escape of contact inhibition and maintain aberrant cell proliferation. Such Drp1-driven regulation of CycE recruitment to mitochondria might be a mechanism to modulate CycE degradation during normal developmental processes as well as in tumorigenic events.},
  file = {/Users/malay/local/zotero_data/storage/WKEN4D9R/parker2015-a_new_mitochondrial_pool_of_cyclin_e,_regulated_by_drp1,_is_linked_to.pdf},
  journal = {J. Cell. Sci.},
  language = {eng},
  number = {22},
  pmcid = {PMC4712782},
  note = {PMID: 26446260}
}

@article{tian2015,
  title = {Computational Methods and Resources for the Interpretation of Genomic Variants in Cancer},
  author = {Tian R. and \textbf{Basu M. K.} and Capriotti E.},
  year = {2015},
  volume = {16 Suppl 8},
  pages = {S7},
  issn = {1471-2164},
  doi = {10.1186/1471-2164-16-S8-S7},
  abstract = {The recent improvement of the high-throughput sequencing technologies is having a strong impact on the detection of genetic variations associated with cancer. Several institutions worldwide have been sequencing the whole exomes and or genomes of cancer patients in the thousands, thereby providing an invaluable collection of new somatic mutations in different cancer types. These initiatives promoted the development of methods and tools for the analysis of cancer genomes that are aimed at studying the relationship between genotype and phenotype in cancer. In this article we review the online resources and computational tools for the analysis of cancer genome. First, we describe the available repositories of cancer genome data. Next, we provide an overview of the methods for the detection of genetic variation and computational tools for the prioritization of cancer related genes and causative somatic variations. Finally, we discuss the future perspectives in cancer genomics focusing on the impact of computational methods and quantitative approaches for defining personalized strategies to improve the diagnosis and treatment of cancer.},
  file = {/Users/malay/local/zotero_data/storage/F8UYB3C3/tian2015-computational_methods_and_resources_for_the_interpretation_of_genomic_variants.pdf},
  journal = {BMC Genomics},
  language = {eng},
  pmcid = {PMC4480958},
  note = {PMID: 26111056}
}

@article{tian2014,
  title = {{{ContrastRank}}: A New Method for Ranking Putative Cancer Driver Genes and Classification of Tumor Samples},
  shorttitle = {{{ContrastRank}}},
  author = {Tian R. and \textbf{Basu M. K.} and Capriotti E.},
  year = {2014},
  month = sep,
  volume = {30},
  pages = {i572-578},
  issn = {1367-4811},
  doi = {10.1093/bioinformatics/btu466},
  abstract = {MOTIVATION: The recent advance in high-throughput sequencing technologies is generating a huge amount of data that are becoming an important resource for deciphering the genotype underlying a given phenotype. Genome sequencing has been extensively applied to the study of the cancer genomes. Although a few methods have been already proposed for the detection of cancer-related genes, their automatic identification is still a challenging task. Using the genomic data made available by The Cancer Genome Atlas Consortium (TCGA), we propose a new prioritization approach based on the analysis of the distribution of putative deleterious variants in a large cohort of cancer samples. RESULTS: In this paper, we present ContastRank, a new method for the prioritization of putative impaired genes in cancer. The method is based on the comparison of the putative defective rate of each gene in tumor versus normal and 1000 genome samples. We show that the method is able to provide a ranked list of putative impaired genes for colon, lung and prostate adenocarcinomas. The list significantly overlaps with the list of known cancer driver genes previously published. More importantly, by using our scoring approach, we can successfully discriminate between TCGA normal and tumor samples. A binary classifier based on ContrastRank score reaches an overall accuracy {$>$}90\% and the area under the curve (AUC) of receiver operating characteristics (ROC) {$>$}0.95 for all the three types of adenocarcinoma analyzed in this paper. In addition, using ContrastRank score, we are able to discriminate the three tumor types with a minimum overall accuracy of 77\% and AUC of 0.83. CONCLUSIONS: We describe ContrastRank, a method for prioritizing putative impaired genes in cancer. The method is based on the comparison of exome sequencing data from different cohorts and can detect putative cancer driver genes. ContrastRank can also be used to estimate a global score for an individual genome about the risk of adenocarcinoma based on the genetic variants information from a whole-exome VCF (Variant Calling Format) file. We believe that the application of ContrastRank can be an important step in genomic medicine to enable genome-based diagnosis. AVAILABILITY AND IMPLEMENTATION: The lists of ContrastRank scores of all genes in each tumor type are available as supplementary materials. A webserver for evaluating the risk of the three studied adenocarcinomas starting from whole-exome VCF file is under development. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.},
  file = {/Users/malay/local/zotero_data/storage/VKRGN9LF/tian2014-contrastrank.pdf},
  journal = {Bioinformatics},
  language = {eng},
  number = {17},
  pmcid = {PMC4147919},
  note = {PMID: 25161249}
}

@article{meli2020,
  title = {{{IL}}-4-Induced Hysteresis in Na\"ive {{T}} Cell Activation},
  author = {Meli A. P. and Wang Y. and {de} Kouchkovsky D. A. and Kong Y. and \textbf{Basu M. K.} and Ghosh S. and Rothlin C. V.},
  year = {2020},
  month = sep,
  pages = {2020.08.31.275842},
  publisher = {{Cold Spring Harbor Laboratory}},
  doi = {10.1101/2020.08.31.275842},
  abstract = {{$<$}h3{$>$}Abstract{$<$}/h3{$>$} {$<$}p{$>$}Na\"ive T cells are generally considered to be a homogeneous population, but for their unique T cell receptors (TCRs). Na\"ive T cells are activated within a specific cytokine milieu upon interaction with antigen-presenting cells through cognate TCR::MHC-peptide interaction and co-stimulation. Here we demonstrate that na\"ive T cells are transcriptionally heterogeneous, and that the relative proportions of transcriptionally distinct na\"ive T cell subpopulations are modified by immune responses, such as during helminth infection. Not only are cognate na\"ive T cells activated during an immune response, but the cytokine produced - such as IL-4 during helminth infection - changes the transcriptome of bystander na\"ive T cells. Such changes in gene expression and population level heterogeneity in bystander na\"ive T cells result in altered responses to a concurrent immune challenge, for instance, hypo-responsiveness to vaccination. Thus, na\"ive T cell activation is not the result of a singular temporal event, but is characterized by hysteresis. Our studies suggest that antigen-agnostic, cytokine-dependent na\"ive T cell conditioning and resulting hysteresis is a mechanism that integrates input signals from concurrent infections for the regulation of the overall magnitude of the immune response.{$<$}/p{$>$}},
  chapter = {New Results},
  copyright = {\textcopyright{} 2020, Posted by Cold Spring Harbor Laboratory. The copyright holder for this pre-print is the author. All rights reserved. The material may not be redistributed, re-used or adapted without the author's permission.},
  file = {/Users/malay/local/zotero_data/storage/D3IGMMYS/meli2020-il-4-induced_hysteresis_in_naive_t_cell_activation.pdf},
  journal = {bioRxiv},
  language = {en},
  note = {doi: https://doi.org/10.1101/2020.08.31.275842}
}

@article{spurlock2021,
  title = {Fine-Tuned Repression of {{Drp1}}-Driven Mitochondrial Fission Primes a `Stem/Progenitor-like State' to Support Neoplastic Transformation},
  author = {Spurlock B. and Parker D. and \textbf{Basu M. K.} and Hjelmeland A. and GC S. and Liu S. and Siegal G. P. and Gunter A. and Moran A. and Mitra K.},
  editor = {Banerjee, Utpal},
  year = {2021},
  month = sep,
  journal = {eLife},
  volume = {10},
  pages = {e68394},
  publisher = {{eLife Sciences Publications, Ltd}},
  issn = {2050-084X},
  doi = {10.7554/eLife.68394},
  file = {/Users/malay/local/zotero_data/storage/9KVE5HJI/spurlock2021-fine-tuned_repression_of_drp1-driven_mitochondrial_fission_primes_a.pdf}
}

@article{suster2022,
  title = {Atypical Thymomas with Squamoid and Spindle Cell Features: Clinicopathologic, Immunohistochemical and Molecular Genetic Study of 120 Cases with Long-Term Follow-Up},
  shorttitle = {Atypical Thymomas with Squamoid and Spindle Cell Features},
  author = {Suster D. I. and Craig Mackinnon A. and DiStasio M. and \textbf{Basu M. K.} and Pihan G, and Suster S.},
  year = {2022},
  month = feb,
  journal = {Mod Pathol},
  issn = {1530-0285},
  doi = {10.1038/s41379-022-01013-x},
  abstract = {Thymomas are rare tumors characterized by a broad range of morphologic appearances that can sometimes give rise to difficulties for classification. We have studied a series of 120 thymoma patients in whom the tumors were characterized by sheets of atypical epithelial cells with squamoid and/or spindle cell features. They occurred in 63 men and 57 women and presented as a discrete mass in the anterior mediastinum measuring 2-23\,cm (mean: 8.2\,cm). Patients' ages ranged from 14 to 86 years (mean: 57.8) and most had symptoms referable to a mass lesion. 20 patients had myasthenia gravis or other autoimmune disorder. 76 cases were characterized by a predominant population of round to polygonal tumor cells while 32 cases were characterized by atypical oval or spindle cells. 12 cases showed mixed features and 16 cases showed the development of thymic carcinoma arising from thymoma. All cases were positive for p40/p63 and cytokeratin AE1/AE3. 23 cases were positive for CD5 (25\%), and 13 for CD117 (14\%). MIB1 showed a significant increase in proliferative activity (mean\,=\,11.6\%). Next generation sequencing in 47 cases did not disclose any variants amenable to current targeted therapies. Clinical follow up ranging from 2 to 29 years showed a progressive increase in aggressive behavior and fatality rate with advancing stage. Overall survival was 87\% at 5 years, 67\% at 10 years, and 23\% at 20 years. Completeness of resection and staging were the most significant parameters for survival. The more aggressive tumors followed a protracted clinical course with multiple recurrences and metastases over a long period of time (mean\,=\,19.8 years from time of initial relapse to death). Atypical thymomas are a distinct category of thymic epithelial neoplasm characterized by a slowly progressive clinical course with increased potential for metastases, transformation to a higher-grade malignancy, and fatal outcome in some cases.},
  langid = {english},
  pmid = {35145198}
}

Swenson-Fields KI, Ward CJ, Lopez ME, Fross S, Heimes Dillon AL, Meisenheimer JD, Rabbani AJ, Wedlock E, Basu MK, Jansson KP, Rowe PS, Stubbs JR, Wallace DP, Vitek MP, Fields TA. Caspase-1 and the inflammasome promote polycystic kidney disease progression. Front Mol Biosci. 2022 Nov 29;9:971219. doi: 10.3389/fmolb.2022.971219. PMID: 36523654; PMCID: PMC9745047.

@article{swenson2022,
  title = {Caspase-1 and the inflammasome promote polycystic kidney disease progression},
  author = {Swenson-Fields K.I. and Ward C. J. and Lopez M. E. and Fross S. and Heimes Dillon A. L. and Meisenheimer J. D. and  Rabbani A. J. and Wedlock E. and \textbf{Basu M. K.} and Jansson K. P. and  Rowe P. S. and Stubbs J. R. and Wallace D. P. and Vitek M. P. and Fields T. A.},
  year = {2022},
  month = Nov,
  volume = {9},
  pages = {971219},
  journal = {Front Mol Biosci},
  doi = {10.3389/fmolb.2022.971219},
  abstract = {},
  langid = {english},
  pmid = {36523654}, 
  note = {doi: 10.3389/fmolb.2022.971219 PMID: 36523654}
}