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Transcription factors (TFs)
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Pre-computed TF profiles
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Transcription factors (TFs)
Help
Target genes
Help
Regulatory sequences Help
Pre-computed TF profiles
Help
Transcription factors (TFs)
Help
Target genes
Help
Regulatory sequences Help
Pre-computed TF profiles
Help
Transcription factors (TFs)
Help
Target genes
Help
Regulatory sequences Help
Pre-computed TF profiles
Help
Browse projects
Transcription factors (TFs)
Help
Target genes
Help
Regulatory sequences Help
Pre-computed TF profiles
Help
.
Welcome to PAZAR!
PAZAR is your one stop shopping experience for transcription factors and regulatory sequence annotations. It is a software framework for the construction and maintenance of regulatory sequence data annotations; a framework which allows multiple boutique databases to function independently within a larger system (or information mall). Our goal is to be the public repository for regulatory data. View our publications »

View our past webinars (latest: January 25, 2012)

Profiles
Seqs
Genes
TFs
Public projects

9
4
1
Activity of the amyloid beta peptide (Alzheimer's associated) as a transcription factor
611
205
152
ABS: a database of Annotated regulatory Binding Sites from orthologous promoters E. Blanco, D. Farré, M. Albà, X. Messeguer and R. Guigó. ABS: a database of Annotated regulatory Binding Sites from orthologous promoters. Nucleic Acids Research 34:D63-D67 (2006). http://genome.imim.es/datasets/abs2005 http://nar.oxfordjournals.org/cgi/content/full/34/suppl_1/D63
32,297
13,918
1
Tan SK, Lin ZH, Chang CW, Varang V et al. AP-2γ regulates oestrogen receptor-mediated long-range chromatin interaction and gene transcription. EMBO J 2011 May 13;30(13):2569-81. AP-2γ ChIP sequencing in E2 (estradiol) treated MCF-7 cells
4,552
1,996
0
Tan SK, Lin ZH, Chang CW, Varang V et al. AP-2γ regulates oestrogen receptor-mediated long-range chromatin interaction and gene transcription. EMBO J 2011 May 13;30(13):2569-81. AP-2γ ChIP sequencing in ETOH (ethanol) treated MCF-7 cells
205
193
1
AR (C)
20
20
1
The ARE project contains twenty active antioxidant responsive elements (AREs) that are a subset of the AREs originally curated in Wang et al, 2007, Table S1 (PMID: 17409198). Active AREs were selected by Chou and Wasserman (unpublished results) and bulk-uploaded with the interacting transcription factor labeled as human NFE2L2 (NRF2). Consult each original publication to determine the actual species source of TF used in the experiments. The NFE2L2 protein interacts with one of the small Maf proteins to form a functional complex.
19,225
8,112
1
The proneural, basic helix-loop-helix transcription factor Atoh1 governs the development of numerous key neuronal subtypes, such as cerebellar granule and brainstem neurons, inner ear hair cells, and several neurons of the proprioceptive system, as well as diverse nonneuronal cell types, such as Merkel cells and intestinal secretory lineages. However, the mere handful of targets that have been identified barely begin to account for Atoh1's astonishing range of functions, which also encompasses seemingly paradoxical activities, such as promoting cell proliferation and medulloblastoma formation in the cerebellum and inducing cell cycle exit and suppressing tumorigenesis in the intestine. We used a multipronged approach to create a comprehensive, unbiased list of over 600 direct Atoh1 target genes in the postnatal cerebellum. We found that Atoh1 binds to a 10 nucleotide motif (AtEAM) to directly regulate genes involved in migration, cell adhesion, metabolism, and other previously unsuspected functions. This study expands current thinking about the transcriptional activities driving neuronal differentiation and provides a framework for further neurodevelopmental studies.
84
82
1
BACH1_ (C)
Warnatz HJ, Schmidt D, Manke T, Piccini I et al. The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle. J Biol Chem 2011 Jul 1;286(26):23521-32. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.
29,878
12,414
1
Hu G, Schones DE, Cui K, Ybarra R et al. Regulation of nucleosome landscape and transcription factor targeting at tissue-specific enhancers by BRG1. Genome Res 2011 Oct;21(10):1650-8. In this report, we identify GATA1-bound enhancers genome-wide and find a global reorganization of the nucleosomes at these enhancers during differentiation of hematopoietic stem cells (HSCs) to erythrocytes. We show that the catalytic subunit BRG1 of BAF complexes localizes to these enhancers during differentiation and generates a longer nucleosome repeat length surrounding the GATA1 sites by shifting the flanking nucleosomes away. Intriguing, we find that the nucleosome shifting specifically facilitates binding of TAL1 but not GATA1, which subsequently activates transcription of target genes.
31,816
12,008
1
Hu G, Schones DE, Cui K, Ybarra R et al. Regulation of nucleosome landscape and transcription factor targeting at tissue-specific enhancers by BRG1. Genome Res 2011 Oct;21(10):1650-8. In this report, we identify GATA1-bound enhancers genome-wide and find a global reorganization of the nucleosomes at these enhancers during differentiation of hematopoietic stem cells (HSCs) to erythrocytes. We show that the catalytic subunit BRG1 of BAF complexes localizes to these enhancers during differentiation and generates a longer nucleosome repeat length surrounding the GATA1 sites by shifting the flanking nucleosomes away. Intriguing, we find that the nucleosome shifting specifically facilitates binding of TAL1 but not GATA1, which subsequently activates transcription of target genes.
20
13
14
Genes approved for MaxiPromoter Desgin in CanEuCre. CART data were submitted under TFe project prior to the opening of this project.
9,998
6,261
1
Cao (C)
Cao AR, Rabinovich R, Xu M, Xu X et al. Genome-wide analysis of transcription factor E2F1 mutant proteins reveals that N- and C-terminal protein interaction domains do not participate in targeting E2F1 to the human genome. J Biol Chem 2011 Apr 8;286(14):11985-96. First, we performed ChIP-seq for tagged WT E2F1. Then, we analyzed E2F1 proteins that lacked the N-terminal SP1 and cyclin A binding domains, the C-terminal transactivation and pocket protein binding domains, and the internal marked box domain. Surprisingly, we found that the ChIP-seq patterns of the mutant proteins were identical to that of WT E2F1.
59,098
16,460
1
To examine transcription factor (TF) network(s), we created mouse ESC lines, in each of which 1 of 50 TFs tagged with a FLAG moiety is inserted into a ubiquitously controllable tetracycline-repressible locus. Of the 50 TFs, Cdx2 provoked the most extensive transcriptome perturbation in ESCs, followed by Esx1, Sox9, Tcf3, Klf4, and Gata3. ChIP-Seq revealed that CDX2 binds to promoters of upregulated target genes. By contrast, genes downregulated by CDX2 did not show CDX2 binding but were enriched with binding sites for POU5F1, SOX2, and NANOG. Genes with binding sites for these core TFs were also downregulated by the induction of at least 15 other TFs, suggesting a common initial step for ESC differentiation mediated by interference with the binding of core TFs to their target genes. These ESC lines provide a fundamental resource to study biological networks in ESCs and mice.
30,409
12,334
1
Schmidt D, Schwalie PC, Ross-Innes CS, Hurtado A et al. A CTCF-independent role for cohesin in tissue-specific transcription. Genome Res 2010 May;20(5):578-88. ChIP-Seq study in human HEPG2 cells using antibodies against CEBPa
113,080
39,054
2
Transcription factors (TFs) direct gene expression by binding to DNA regulatory regions. To explore the evolution of gene regulation, we used chromatin immunoprecipitation with high-throughput sequencing (ChIP-seq) to determine experimentally the genome-wide occupancy of two TFs, CCAAT/enhancer-binding protein alpha and hepatocyte nuclear factor 4 alpha, in the livers of five vertebrates. Although each TF displays highly conserved DNA binding preferences, most binding is species-specific, and aligned binding events present in all five species are rare. Regions near genes with expression levels that are dependent on a TF are often bound by the TF in multiple species yet show no enhanced DNA sequence constraint. Binding divergence between species can be largely explained by sequence changes to the bound motifs. Among the binding events lost in one lineage, only half are recovered by another binding event within 10 kilobases. Our results reveal large interspecies differences in transcriptional regulation and provide insight into regulatory evolution.
0
0
0
25,381
13,268
1
Hu G, Schones DE, Cui K, Ybarra R et al. Regulation of nucleosome landscape and transcription factor targeting at tissue-specific enhancers by BRG1. Genome Res 2011 Oct;21(10):1650-8. CTCF CHipseq data
45,418
16,918
1
93
54
15
Gene regulation in diabetes
6,487
6,822
1
The E2F family of transcription factors has important roles in cell cycle progression. E2F4 is an E2F family member that has been proposed to be primarily a repressor of transcription, but the scope of its binding activity and functions in transcriptional regulation is not fully known. We used ChIP sequencing (ChIP-seq) to identify around 16 000 E2F4 binding sites which potentially regulate 7346 downstream target genes with wide-ranging functions in DNA repair, cell cycle regulation, apoptosis, and other processes. While half of all E2F4 binding sites (56%) occurred near transcription start sites (TSSs), ¡­20% of sites occurred more than 20 kb away from any annotated TSS. These distal sites showed histone modifications suggesting that E2F4 may function as a long-range regulator, which we confirmed by functional experimental assays on a subset. Overexpression of E2F4 and its transcriptional cofactors of the retinoblastoma (Rb) family and its binding partner DP-1 revealed that E2F4 acts as an activator as well as a repressor. E2F4 binding sites also occurred near regulatory elements for miRNAs such as let-7a and mir-17, suggestive of regulation of miRNAs by E2F4. Taken together, our genome-wide analysis provided evidence of versatile roles of E2F4 and insights into its functions.
9,339
6,205
1
The transcription factor early B cell factor-1 (Ebf1) is a key determinant of B lineage specification and differentiation. To gain insight into the molecular basis of Ebf1 function in early-stage B cells, we combined a genome-wide ChIP sequencing analysis with gain- and loss-of-function transcriptome analyses. Among 565 genes that are occupied and transcriptionally regulated by Ebf1, we identified large sets involved in (pre)-B cell receptor and Akt signaling, cell adhesion, and migration. Interestingly, a third of previously described Pax5 targets was found to be occupied by Ebf1. In addition to Ebf1-activated and -repressed genes, we identified targets at which Ebf1 induces chromatin changes that poise the genes for expression at subsequent stages of differentiation. Poised chromatin states on specific targets could also be established by Ebf1 expression in T cells but not in NIH 3T3 cells, suggesting that Ebf1 acts as a "pioneer" factor in a hematopoietic chromatin context.
35,338
12,995
1
Early growth response gene 1 (EGR1) has been implicated in megakaryocyte differentiation induced by phorbol ester. But the molecule mechanism of EGR1 in this process has not been widely investigated. The identification of direct EGR1 target genes in a global scale is critical for our understanding of how EGR1 contributes to this process. In this study, we provide a global survey on the binding location of EGR1 in the K562 cells using chromatin immunoprecipitation and massively parallel sequencing. Over 14 000 highly confident in vivo EGR1 binding sites were identified in phorbol 12-myristate 13-acetate-treated K562 cells. More than 70% of these genomic sites associated with EGR1 binding were located around annotated gene regions. Molecular functional classification of 6138 putative EGR1 target genes showed that the transcription factor class (695 of 6138; 11%) is the largest significantly enriched one. The results showed that a high coverage of the genome and a high positive rate achieve were achieved. This whole genome study on the EGR1 targets may provide a better understanding of the EGR1 regulated genes and the downstream pathway in megakaryocyte differentiation.
301
281
1
Schödel J, Oikonomopoulos S, Ragoussis J, Pugh CW et al. High-resolution genome-wide mapping of HIF-binding sites by ChIP-seq. Blood 2011 Jun 9;117(23):e207-17. Using chromatin immunoprecipitation linked to high throughput sequencing, we identify HIF-binding sites across the genome, independently of gene architecture
11,192
5,713
1
Nuclear receptor estrogen receptor alpha (ER alpha) controls the expression of hundreds of genes responsible for target cell phenotypic properties, but the relative importance of direct versus tethering mechanisms of DNA binding has not been established. In this first report, we examine the genome-wide chromatin localization of an altered-specificity mutant ER with a DNA binding domain deficient in binding to estrogen response element (ERE)-containing DNA (DBDmut ER) versus wild-type ER alpha. Using high-throughput sequencing of ER chromatin immunoprecipitations (ChIP-Seq) and mRNA transcriptional profiling, we show that direct ERE binding is required for most of (75%) estrogen-dependent gene regulation and 90% of hormone-dependent recruitment of ER to genomic binding sites.
22,150
10,460
1
ESR1 (C)
3,557
2,045
1
Cicatiello L, Mutarelli M, Grober OM, Paris O, Ferraro L, Ravo M, Tarallo R, Luo S, Schroth GP, Seifert M, Zinser C, Chiusano ML, Traini A, De Bortoli M, Weisz A. Estrogen receptor alpha controls a gene network in luminal-like breast cancer cells comprising multiple transcription factors and microRNAs. Am J Pathol. 2010 May;176(5):2113-30. Epub 2010 Mar 26.
6,024
3,577
1
Grober OM, Mutarelli M, Giurato G, Ravo M, Cicatiello L, De Filippo MR, Ferraro L, Nassa G, Papa MF, Paris O, Tarallo R, Luo S, Schroth GP, Benes V, Weisz A. Global analysis of estrogen receptor beta binding to breast cancer cell genome reveals an extensive interplay with estrogen receptor alpha for target gene regulation. BMC Genomics. 2011 Jan 14;12:36.
9,701
5,307
1
Grober OM, Mutarelli M, Giurato G, Ravo M, Cicatiello L, De Filippo MR, Ferraro L, Nassa G, Papa MF, Paris O, Tarallo R, Luo S, Schroth GP, Benes V, Weisz A. Global analysis of estrogen receptor beta binding to breast cancer cell genome reveals an extensive interplay with estrogen receptor alpha for target gene regulation. BMC Genomics. 2011 Jan 14;12:36.
14,815
10,843
1
To uncover the sequence motifs that mediate specific functions of ETS1, a genome-wide approach, chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq), identified both promoter and enhancer binding events in Jurkat T cells. A comparison with DNase I sensitivity both validated the dataset and also improved accuracy. Redundant occupancy of ETS1 with the ETS protein GABPA occurred primarily in promoters of housekeeping genes, whereas ETS1 specific occupancy occurred in the enhancers of T cell-specific genes. Two routes to ETS1 specificity were identified: an intrinsic preference of ETS1 for a variant of the ETS family consensus sequence and the presence of a composite sequence that can support cooperative binding with a RUNX transcription factor.
4,502
1,978
1
Polycomb Repressive Complex 2 (PRC2) regulates key developmental genes in embryonic stem (ES) cells and during development. Here we show that Jarid2/Jumonji, a protein enriched in pluripotent cells and a founding member of the Jumonji C (JmjC) domain protein family, is a PRC2 subunit in ES cells. Genome-wide ChIP-seq analyses of Jarid2, Ezh2, and Suz12 binding reveal that Jarid2 and PRC2 occupy the same genomic regions. We further show that Jarid2 promotes PRC2 recruitment to the target genes while inhibiting PRC2 histone methyltransferase activity, suggesting that it acts as a "molecular rheostat" that finely calibrates PRC2 functions at developmental genes. Using Xenopus laevis as a model we demonstrate that Jarid2 knockdown impairs the induction of gastrulation genes in blastula embryos and results in failure of differentiation. Our findings illuminate a mechanism of histone methylation regulation in pluripotent cells and during early cell-fate transitions.
18,190
10,376
1
Transcription of the eukaryotic genomes is carried out by three distinct RNA polymerases I, II, and III, whereby each polymerase is thought to independently transcribe a distinct set of genes. To investigate a possible relationship of RNA polymerases II and III, we mapped their in vivo binding sites throughout the human genome by using ChIP-Seq in two different cell lines, GM12878 and K562 cells. Pol III was found to bind near many known genes as well as several previously unidentified target genes. RNA-Seq studies indicate that a majority of the bound genes are expressed, although a subset are not suggestive of stalling by RNA polymerase III. Pol II was found to bind near many known Pol III genes, including tRNA, U6, HVG, hY, 7SK and previously unidentified Pol III target genes. Similarly, in vivo binding studies also reveal that a number of transcription factors normally associated with Pol II transcription, including c-Fos, c-Jun and c-Myc, also tightly associate with most Pol III-transcribed genes. Inhibition of Pol II activity using alpha-amanitin reduced expression of a number of Pol III genes (e.g., U6, hY, HVG), suggesting that Pol II plays an important role in regulating their transcription. These results indicate that, contrary to previous expectations, polymerases can often work with one another to globally coordinate gene expression.
35,868
11,907
1
36,426
11,884
1
Tan SK, Lin ZH, Chang CW, Varang V et al. AP-2γ regulates oestrogen receptor-mediated long-range chromatin interaction and gene transcription. EMBO J 2011 May 13;30(13):2569-81. FoxA1 ChIP sequencing in ETOH (ethanol) treated MCF-7 cells
4,197
3,860
1
4,184
2,590
1
The transcription factor GATA-1 is required for terminal erythroid maturation and functions as an activator or repressor depending on gene context. Yet its in vivo site selectivity and ability to distinguish between activated versus repressed genes remain incompletely understood. In this study, we performed GATA-1 ChIP-seq in erythroid cells and compared it to GATA-1-induced gene expression changes. Bound and differentially expressed genes contain a greater number of GATA-binding motifs, a higher frequency of palindromic GATA sites, and closer occupancy to the transcriptional start site versus nondifferentially expressed genes. Moreover, we show that the transcription factor Zbtb7a occupies GATA-1-bound regions of some direct GATA-1 target genes, that the presence of SCL/TAL1 helps distinguish transcriptional activation versus repression, and that polycomb repressive complex 2 (PRC2) is involved in epigenetic silencing of a subset of GATA-1-repressed genes. These data provide insights into GATA-1-mediated gene regulation in vivo.
15,529
6,575
1
Linnemann AK, O'Geen H, Keles S, Farnham PJ et al. Genetic framework for GATA factor function in vascular biology. Proc Natl Acad Sci U S A 2011 Aug 16;108(33):13641-6. we used ChIP-seq and loss-of-function strategies to define the GATA-2-instigated genetic network in human endothelial cells. By contrast to erythroid cells, GATA-2 occupied a unique target gene ensemble, consisting of genes encoding key determinants of endothelial cell identity and inflammation. GATA-2-occupied sites characteristically contained motifs that bind Activator Protein-1 (AP-1), a pivotal regulator of inflammatory genes. GATA-2 frequently occupied the same chromatin sites as c-JUN and c-FOS, heterodimeric components of AP-1. Though all three components were required for maximal AP-1 target gene expression, GATA-2 was not required for AP-1 chromatin occupancy. GATA-2 conferred maximal phosphorylation of chromatin-bound c-JUN at Ser 73, which stimulates AP-1-dependent transactivation, in a chromosomal context-dependent manner.
20,704
9,017
1
Kong SL, Li G, Loh SL, Sung WK et al. Cellular reprogramming by the conjoint action of ERα, FOXA1, and GATA3 to a ligand-inducible growth state. Mol Syst Biol 2011 Aug 30;7:526. The analysis of GATA3 in MCF-7 cancer cells was done by ChIP-seq data obtained either with estradiol (E2) stimulation"
80
55
1
Compilation of binding sites for the HIF1 transcription factor complex composed of HIF1A and ARNT. The data was extracted from the following review: [DOI: 10.1126/stke.3062005re12] Roland H. Wenger, Daniel P. Stiehl and Gieri Camenisch. Integration of oxygen signaling at the consensus HRE. (2005) Sci STKE. 306:re12.
349
334
1
Schödel J, Oikonomopoulos S, Ragoussis J, Pugh CW et al. High-resolution genome-wide mapping of HIF-binding sites by ChIP-seq. Blood 2011 Jun 9;117(23):e207-17. Using chromatin immunoprecipitation linked to high throughput sequencing, we identify HIF-binding sites across the genome, independently of gene architecture
387
443
1
Hypoxia-inducible factor 1 (HIF-1) plays a key role in cellular adaptation to hypoxia. To better understand the determinants of HIF-1 binding and transactivation, we used ChIP-chip and gene expression profiling to define the relationship between the epigenetic landscape, sites of HIF-1 binding, and genes transactivated by hypoxia in two cell lines.
107
79
1
The HNF4 project houses data from the Sladek lab at UC Riverside (http://www.sladeklab.ucr.edu/). The project includes 107 expert curated TFBS that were bulk-uploaded with the interacting transcription factor labeled as human HNF4A. Consult each original publication to determine the actual species source of TF used in the experiments. H4 numbers assigned to regulatory sequences refer to specific binding sites.
8,307
3,032
0
Schmidt D, Schwalie PC, Ross-Innes CS, Hurtado A et al. A CTCF-independent role for cohesin in tissue-specific transcription. Genome Res 2010 May;20(5):578-88.ChIP-Seq study in human HEFG2 cells using antibodies against HNF4A
25,081
10,841
1
23,344
10,181
1
586
151
1
IGF1R (C)
586
138
1
The insulin-like growth factor 1 receptor (IGF-1R) plays crucial roles in developmental and cancer biology. Most of its biological effects have been ascribed to its tyrosine kinase activity, which propagates signaling through the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways. Here, we report that IGF-1 promotes the modification of IGF-1R by small ubiquitin-like modifier protein-1 (SUMO-1) and its translocation to the nucleus. Nuclear IGF-1R associated with enhancer-like elements and increased transcription in reporter assays. The SUMOylation sites of IGF-1R were identified as three evolutionarily conserved lysine residues-Lys(1025), Lys(1100), and Lys(1120)-in the beta subunit of the receptor. Mutation of these SUMO-1 sites abolished the ability of IGF-1R to translocate to the nucleus and activate transcription but did not alter its kinase-dependent signaling. Thus, we demonstrate a SUMOylation-mediated mechanism of IGF-1R signaling that has potential implications for gene regulation
3,372
1,522
1
Polycomb Repressive Complex 2 (PRC2) regulates key developmental genes in embryonic stem (ES) cells and during development. Here we show that Jarid2/Jumonji, a protein enriched in pluripotent cells and a founding member of the Jumonji C (JmjC) domain protein family, is a PRC2 subunit in ES cells. Genome-wide ChIP-seq analyses of Jarid2, Ezh2, and Suz12 binding reveal that Jarid2 and PRC2 occupy the same genomic regions. We further show that Jarid2 promotes PRC2 recruitment to the target genes while inhibiting PRC2 histone methyltransferase activity, suggesting that it acts as a "molecular rheostat" that finely calibrates PRC2 functions at developmental genes. Using Xenopus laevis as a model we demonstrate that Jarid2 knockdown impairs the induction of gastrulation genes in blastula embryos and results in failure of differentiation. Our findings illuminate a mechanism of histone methylation regulation in pluripotent cells and during early cell-fate transitions.
138
3,504
1
96
The JASPAR CORE database contains a curated, non-redundant set of 123 transcription factor binding profiles from published articles. JASPAR website is : http://jaspar.genereg.net
1,356
1,220
1
KLF1 regulates a diverse suite of genes to direct erythroid cell differentiation from bipotent progenitors. To determine the local cis-regulatory contexts and transcription factor networks in which KLF1 operates, we performed KLF1 ChIP-seq in the mouse. We found at least 945 sites in the genome of E14.5 fetal liver erythroid cells which are occupied by endogenous KLF1. Many of these recovered sites reside in erythroid gene promoters such as Hbb-b1, but the majority are distant to any known gene. Our data suggests KLF1 directly regulates most aspects of terminal erythroid differentiation including production of alpha- and beta-globin protein chains, heme biosynthesis, coordination of proliferation and anti-apoptotic pathways, and construction of the red cell membrane and cytoskeleton by functioning primarily as a transcriptional activator. Additionally, we suggest new mechanisms for KLF1 cooperation with other transcription factors, in particular the erythroid transcription factor GATA1, to maintain homeostasis in the erythroid compartment.
62
14
0
Set of liver-specific regulatory regions and transcription factor binding sites curated from the literature
400
409
1
MEIS1 (C)
12,139
7,040
2
Malignant melanoma is an aggressive cancer known for its notorious resistance to most current therapies. The basic helix-loop-helix microphthalmia transcription factor (MITF) is the master regulator determining the identity and properties of the melanocyte lineage, and is regarded as a lineage-specific ‘oncogene’ that has a critical role in the pathogenesis of melanoma. MITF promotes melanoma cell proliferation, whereas sustained supression of MITF expression leads to senescence. By combining chromatin immunoprecipitation coupled to high throughput sequencing (ChIP-seq) and RNA sequencing analyses, we show that MITF directly regulates a set of genes required for DNA replication, repair and mitosis. Our results reveal how loss of MITF regulates mitotic fidelity, and through defective replication and repair induces DNA damage, ultimately ending in cellular senescence. These findings reveal a lineage-specific control of DNA replication and mitosis by MITF, providing new avenues for therapeutic intervention in melanoma. The identification of MITF-binding sites and gene-regulatory networks establish a framework for understanding oncogenic basic helix-loop-helix factors such as N-myc or TFE3 in other cancers.
23
2
13
Sequences regulating the transcription of the Mucin 5AC MUC5AC gene.
49
15
0
Set of muscle-specific regulatory regions and transcription factor binding sites curated from the literature.
116
29
38
The NFIRegulomeDB is a database of genes regulated by the Nuclear Factor I transcription factor family compiled by the Gronostajski Lab. The long-term goal is to provide a generic annotation and search system that individual labs focussed on specific transcription factors or transcription factor families can use to keep databases on genes that their factors regulate. Eventually we'd like to link these individual databases into a distributed RegulomeDB for all known regulated genes and their associated transcription factors. http://nfiregulome.ccr.buffalo.edu
6,903
4,689
1
NR1H (C)
2,926
2,431
1
Somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs) with the introduction of Oct4, Sox2, Klf4, and c-Myc. Among these four factors, Oct4 is critical in inducing pluripotency because no transcription factor can substitute for Oct4, whereas Sox2, Klf4, and c-Myc can be replaced by other factors. Here we show that the orphan nuclear receptor Nr5a2 (also known as Lrh-1) can replace Oct4 in the derivation of iPSCs from mouse somatic cells, and it can also enhance reprogramming efficiency. Sumoylation mutants of Nr5a2 with enhanced transcriptional activity can further increase reprogramming efficiency. Genome-wide location analysis reveals that Nr5a2 shares many common gene targets with Sox2 and Klf4, which suggests that the transcription factor trio works in concert to mediate reprogramming. We also show that Nr5a2 works in part through activating Nanog. Together, we show that unrelated transcription factors can replace Oct4 and uncovers an exogenous Oct4-free reprogramming code.
1,256
1,030
1
NRF2 (C)
NRF2 ChIP-seq data
1,872
1,550
1
In vivo protein-DNA interactions connect each transcription factor with its direct targets to form a gene network scaffold. To map these protein-DNA interactions comprehensively across entire mammalian genomes, we developed a large-scale chromatin immunoprecipitation assay (ChIPSeq) based on direct ultrahigh-throughput DNA sequencing. This sequence census method was then used to map in vivo binding of the neuron-restrictive silencer factor (NRSF; also known as REST, for repressor element-1 silencing transcription factor) to 1946 locations in the human genome. The data display sharp resolution of binding position [+/-50 base pairs (bp)], which facilitated our finding motifs and allowed us to identify noncanonical NRSF-binding motifs. These ChIPSeq data also have high sensitivity and specificity [ROC (receiver operator characteristic) area >/= 0.96] and statistical confidence (P <10(-4)), properties that were important for inferring new candidate interactions. These include key transcription factors in the gene network that regulates pancreatic islet cell development.
25
19
1
Collection of binding sites for Olf/Ebf proteins from the literature.
690
256
111
ORegAnno Dataset. The Open REGulatory ANNOtation database (ORegAnno) is an open database for the curation of known regulatory elements from scientific literature. Annotation is collected from users worldwide for various biological assays. http://www.oreganno.org Montgomery SB, Griffith OL, Sleumer MC, Bergman CM, Bilenky M, Pleasance ED, Prychyna Y, Zhang X and Jones SJM. (2006) ORegAnno: An open access database and curation system for literature-derived promoters, transcription factor binding sites and regulatory variation. Bioinformatics 22(5):637-40.
457
295
0
Stanford ENCODE Dataset. This set was generated by aligning full-length cDNA clones from the Mammalian Gene Collection to the human genome rough draft sequence to estimate the start sites of more than 10,000 human transcripts. Genomic sequence just upstream from the 5' end of these cDNA sequences was selected and designated as putative promoters. Random putative promoter were assayed in a luciferase-based transfection assay in multiple cultured cell types. This dataset was extracted from the ORegAnno database. http://www-shgc.stanford.edu/myerslab Trinklein N, Force Aldred S, Saldanha A, and Myers RM. (2003) Identification and functional analysis of human transcriptional promoters. Genome Research 13(2):308-312.
33
8
1
Mammalian Erythroid Cis-Regulatory Modules. A set of cis regulatory modules for mammalian genes expressed in red blood cells reported by Wang et al (2006) by the Hardison lab at PSU, extracted from the ORegAnno database. http://www.bx.psu.edu/~ross/dataset/DatasetHome.html Wang H, Zhang Y, Cheng Y, Zhou Y, King DC, Taylor J, Chiaromonte F, Kasturi J, Petrykowska H, Gibb B, Dorman C, Miller W, Dore LC, Welch J, Weiss MJ, Hardison RC. 2006. Experimental validation of predicted mammalian erythroid cis-regulatory modules. Genome Res. 16(12):1480-92.
195
192
1
STAT1 ChIP-Seq-derived Binding Sites. A set of transcription factor binding sites for STAT1, extracted from the ORegAnno database. Experimental determination of STAT1 binding sites by ChIP-TS (chromatin immunoprecipitation with tag sequencing by the Illumina 1G system, Bentley DR 2006, PMID: 17055251). Robertson G, Hirst M, Bainbridge M, Bilenky M, Zhao Y, Zeng T, Pandoh P, Fichter K, Tam A, Ma K, Prabhu AL, Moksa M, Lee S, Mah D, Sa D, McDonald H, Delaney A, Theissen N, Bernier B, Griffith O, He A, Varhol R, Euskirchen G, Snyder M, Marra M and Jones SJM. (2007) Genome-wide profiles of STAT1 DNA association in HeLa S3 cells using chromatin immunoprecipitation and massively parallel sequencing. Nat Methods.
37
28
1
STAT1 literature-derived Binding Sites. A set of transcription factor binding sites for STAT1, extracted from the ORegAnno database. These sites were collected from the scientific literature to serve as positive controls in support of the experimental determination of STAT1 binding sites by ChIP-TS (chromatin immunoprecipitation with tag sequencing by the Illumina 1G system, Bentley DR 2006, PMID: 17055251). Robertson G, Hirst M, Bainbridge M, Bilenky M, Zhao Y, Zeng T, Pandoh P, Fichter K, Tam A, Ma K, Prabhu AL, Moksa M, Lee S, Mah D, Sa D, McDonald H, Delaney A, Theissen N, Bernier B, Griffith O, He A, Varhol R, Euskirchen G, Snyder M, Marra M and Jones SJM. (2007) Genome-wide profiles of STAT1 DNA association in HeLa S3 cells using chromatin immunoprecipitation and massively parallel sequencing. Nat Methods. [Epub ahead of print]
352
216
1
Genome-wide identification of hypoxia-inducible factor binding sites and target genes by a probabilistic model integrating transcription-profiling data and in silico binding site prediction. Ortiz-Barahona A, Villar D, Pescador N, Amigo J, del Peso L. Nucleic Acids Res. 2010 Apr;38(7):2332-45. Epub 2010 Jan 8. PMID:20061373
13,759
9,444
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
4,640
4,824
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
15,637
10,047
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
15,308
10,602
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
2,920
2,542
1
The tumor suppressor p53 plays a crucial role in cellular growth control inducing a plethora of different response pathways. The molecular mechanisms that discriminate between the distinct p53-responses have remained largely elusive. Here, we have analyzed the p53-regulated pathways induced by Actinomycin D and Etoposide treatment resulting in more growth arrested versus apoptotic cells respectively. We found that the genome-wide p53 DNA-binding patterns are almost identical upon both treatments notwithstanding transcriptional differences that we observed in global transcriptome analysis. To assess the role of post-translational modifications in target gene choice and activation we investigated the genome-wide level of phosphorylation of Serine 46 of p53 bound to DNA (p53-pS46) and of Serine 15 (p53-pS15). Interestingly, the extent of S46 phosphorylation of p53 bound to DNA is considerably higher in cells directed towards apoptosis while the degree of phosphorylation at S15 remains highly similar. Moreover, our data suggest that following different chemotherapeutical treatments, the amount of chromatin-associated p53 phosphorylated at S46 but not at pS15 is higher on certain apoptosis related target genes. Our data provide evidence that cell fate decisions are not made primarily on the level of general p53 DNA-binding and that post-translationally modified p53 can have distinct DNA-binding characteristics.
2,132
1,964
1
The tumor suppressor p53 plays a crucial role in cellular growth control inducing a plethora of different response pathways. The molecular mechanisms that discriminate between the distinct p53-responses have remained largely elusive. Here, we have analyzed the p53-regulated pathways induced by Actinomycin D and Etoposide treatment resulting in more growth arrested versus apoptotic cells respectively. We found that the genome-wide p53 DNA-binding patterns are almost identical upon both treatments notwithstanding transcriptional differences that we observed in global transcriptome analysis. To assess the role of post-translational modifications in target gene choice and activation we investigated the genome-wide level of phosphorylation of Serine 46 of p53 bound to DNA (p53-pS46) and of Serine 15 (p53-pS15). Interestingly, the extent of S46 phosphorylation of p53 bound to DNA is considerably higher in cells directed towards apoptosis while the degree of phosphorylation at S15 remains highly similar. Moreover, our data suggest that following different chemotherapeutical treatments, the amount of chromatin-associated p53 phosphorylated at S46 but not at pS15 is higher on certain apoptosis related target genes. Our data provide evidence that cell fate decisions are not made primarily on the level of general p53 DNA-binding and that post-translationally modified p53 can have distinct DNA-binding characteristics.
31
2
5
A compilation of Pax6 regulatory regions
1,595
1,410
1
The transcription factor Pax6 is essential for neural stem cell proliferation, multipotency, and neurogenesis in many regions of the central nervous system, including the cerebral cortex. We used Pax6 as an entry point to define the cellular networks controlling neural stem cell self-renewal and neurogenesis in stem cells of the developing mouse cerebral cortex. We identified the genomic binding locations of Pax6 in neocortical stem cells during normal development and ascertained the functional significance of genes that we found to be regulated by Pax6, finding that Pax6 positively and directly regulates cohorts of genes that promote neural stem cell self-renewal, basal progenitor cell genesis, and neurogenesis. Notably, we defined a core network regulating neocortical stem cell decision-making in which Pax6 interacts with three other regulators of neurogenesis, Neurog2, Ascl1, and Hes1. Analyses of the biological function of Pax6 in neural stem cells through phenotypic analyses of Pax6 gain- and loss-of-function mutant cortices demonstrated that the Pax6-regulated networks operating in neural stem cells are highly dosage sensitive. Increasing Pax6 levels drives the system towards neurogenesis and basal progenitor cell genesis by increasing expression of a cohort of basal progenitor cell determinants, including the key transcription factor Eomes/Tbr2, and thus towards neurogenesis at the expense of self-renewal. Removing Pax6 reduces cortical stem cell self-renewal by decreasing expression of key cell cycle regulators, resulting in excess early neurogenesis. We find that the relative levels of Pax6, Hes1, and Neurog2 are key determinants of a dynamic network that controls whether neural stem cells self-renew, generate cortical neurons, or generate basal progenitor cells, a mechanism that has marked parallels with the transcriptional control of embryonic stem cell self-renewal.
4,701
4,137
1
Polycomb group (PcG) proteins are conserved epigenetic transcriptional repressors that control numerous developmental gene expression programs and have recently been implicated in modulating embryonic stem cell (ESC) fate. We identified the PcG protein PCL2 (polycomb-like 2) in a genome-wide screen for regulators of self-renewal and pluripotency and predicted that it would play an important role in mouse ESC-fate determination. Using multiple biochemical strategies, we provide evidence that PCL2 is a Polycomb Repressive Complex 2 (PRC2)-associated protein in mouse ESCs. Knockdown of Pcl2 in ESCs resulted in heightened self-renewal characteristics, defects in differentiation, and altered patterns of histone methylation. Integration of global gene expression and promoter occupancy analyses allowed us to identify PCL2 and PRC2 transcriptional targets and draft regulatory networks. We describe the role of PCL2 in both modulating transcription of ESC self-renewal genes in undifferentiated ESCs as well as developmental regulators during early commitment and differentiation.
1,476
296
321
Approved genes from the Pleiades project www.pleiades.org
0
0
0
Actually I want to find Nanog Transcriprtion factor binding sequences in promoter and enhancer for Nanog,Pou5f1,Sox2,Klf4,Myc Gene Already its known and published in genome level for nanog. when I do analysis with ORCA tool kit I can find all other Transcription factor in TF profiles but not Nanog factor. Its one paper published that I found in Pazar with linked to pubmed but still its not included in ORCA toolkit Cross-regulation of the Nanog and Cdx2 promoters is one paper published but still Nanog Factor binds to all gene which mentioned above i.e Pou5f1, Sox2, Myc, Klf & Nanog I humbly request you to include them as soon as possible Thanks & Regards vakati vinod
48
3
47
Pluripotency related TFBS from literature
6,996
4,419
1
The derivation of human ES cells (hESCs) from human blastocysts represents one of the milestones in stem cell biology. The full potential of hESCs in research and clinical applications requires a detailed understanding of the genetic network that governs the unique properties of hESCs. Here, we report a genome-wide RNA interference screen to identify genes which regulate self-renewal and pluripotency properties in hESCs. Interestingly, functionally distinct complexes involved in transcriptional regulation and chromatin remodelling are among the factors identified in the screen. To understand the roles of these potential regulators of hESCs, we studied transcription factor PRDM14 to gain new insights into its functional roles in the regulation of pluripotency. We showed that PRDM14 regulates directly the expression of key pluripotency gene POU5F1 through its proximal enhancer. Genome-wide location profiling experiments revealed that PRDM14 colocalized extensively with other key transcription factors such as OCT4, NANOG and SOX2, indicating that PRDM14 is integrated into the core transcriptional regulatory network. More importantly, in a gain-of-function assay, we showed that PRDM14 is able to enhance the efficiency of reprogramming of human fibroblasts in conjunction with OCT4, SOX2 and KLF4. Altogether, our study uncovers a wealth of novel hESC regulators wherein PRDM14 exemplifies a key transcription factor required for the maintenance of hESC identity and the reacquisition of pluripotency in human somatic cells.
8,607
3,346
0
133
126
1
Rap1 is a component of the shelterin complex at mammalian telomeres, but its in vivo role in telomere biology has remained largely unknown to date. Here we show that Rap1 deficiency is dispensable for telomere capping but leads to increased telomere recombination and fragility. We generated cells and mice deleted for Rap1; mice with Rap1 deletion in stratified epithelia were viable but had shorter telomeres and developed skin hyperpigmentation in adulthood. By performing chromatin immunoprecipitation coupled with ultrahigh-throughput sequencing, we found that Rap1 binds to both telomeres and to extratelomeric sites through the (TTAGGG)(2) consensus motif. Extratelomeric Rap1-binding sites were enriched at subtelomeric regions, in agreement with preferential deregulation of subtelomeric genes in Rap1-deficient cells. More than 70% of extratelomeric Rap1-binding sites were in the vicinity of genes, and 31% of the genes deregulated in Rap1-null cells contained Rap1-binding sites, suggesting a role for Rap1 in transcriptional control. These findings place a telomere protein at the interface between telomere function and transcriptional regulation.
140
92
11
RARE (C)
Set of retinoic acid response elements (RARE) curated from the literature
4,524
4,196
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
4,214
3,902
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
8,336
6,902
1
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
3,631
2,855
1
To uncover the sequence motifs that mediate specific functions of ETS1, a genome-wide approach, chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq), identified both promoter and enhancer binding events in Jurkat T cells. A comparison with DNase I sensitivity both validated the dataset and also improved accuracy. Redundant occupancy of ETS1 with the ETS protein GABPA occurred primarily in promoters of housekeeping genes, whereas ETS1 specific occupancy occurred in the enhancers of T cell-specific genes. Two routes to ETS1 specificity were identified: an intrinsic preference of ETS1 for a variant of the ETS family consensus sequence and the presence of a composite sequence that can support cooperative binding with a RUNX transcription factor.
6,511
4,586
1
SETDB1 (C)
658
650
14
Transcription factors (TFs) and their specific interactions with targets are crucial for specifying gene-expression programs. To gain insights into the transcriptional regulatory networks in embryonic stem (ES) cells, we use chromatin immunoprecipitation coupled with ultra-high-throughput DNA sequencing (ChIP-seq) to map the locations of 13 sequence-specific TFs (Nanog, Oct4, STAT3, Smad1, Sox2, Zfx, c-Myc, n-Myc, Klf4, Esrrb, Tcfcp2l1, E2f1, and CTCF) and 2 transcription regulators (p300 and Suz12). These factors are known to play different roles in ES-cell biology as components of the LIF and BMP signaling pathways, self-renewal regulators, and key reprogramming factors. Our study provides insights into the integration of the signaling pathways into the ES-cell-specific transcription circuitries. Intriguingly, we find specific genomic regions extensively targeted by different TFs. Collectively, the comprehensive mapping of TF-binding sites identifies important features of the transcriptional regulatory networks that define ES-cell identity.
4,881
3,813
1
Fang X, Yoon JG, Li L, Yu W et al. The SOX2 response program in glioblastoma multiforme: an integrated ChIP-seq, expression microarray, and microRNA analysis. BMC Genomics 2011 Jan 6;12:11. Using ChIP-seq technology, we identified 4883 SOX2 binding regions in the GBM cancer genome. SOX2 binding regions contain the consensus sequence wwTGnwTw that occurred 3931 instances in 2312 SOX2 binding regions
2,977
3,032
1
SPI1 (C)
Species: Human PMID:21241896 note: start and end calculated as 250bp around midpoint
4,534
1,391
0
Schmidt D, Schwalie PC, Ross-Innes CS, Hurtado A et al. A CTCF-independent role for cohesin in tissue-specific transcription. Genome Res 2010 May;20(5):578-88.ChIP-Seq study in human HEFG2 cells using antibodies against HNF4A
10,958
6,470
1
We developed a method, ChIP-sequencing (ChIP-seq), combining chromatin immunoprecipitation (ChIP) and massively parallel sequencing to identify mammalian DNA sequences bound by transcription factors in vivo. We used ChIP-seq to map STAT1 targets in interferon-gamma (IFN-gamma)-stimulated and unstimulated human HeLa S3 cells, and compared the method's performance to ChIP-PCR and to ChIP-chip for four chromosomes. By ChIP-seq, using 15.1 and 12.9 million uniquely mapped sequence reads, and an estimated false discovery rate of less than 0.001, we identified 41,582 and 11,004 putative STAT1-binding regions in stimulated and unstimulated cells, respectively. Of the 34 loci known to contain STAT1 interferon-responsive binding sites, ChIP-seq found 24 (71%). ChIP-seq targets were enriched in sequences similar to known STAT1 binding motifs. Comparisons with two ChIP-PCR data sets suggested that ChIP-seq sensitivity was between 70% and 92% and specificity was at least 95%
36,902
13,082
1
Chromatin immunoprecipitation (ChIP) followed by tag sequencing (ChIP-seq) using high-throughput next-generation instrumentation is fast, replacing chromatin immunoprecipitation followed by genome tiling array analysis (ChIP-chip) as the preferred approach for mapping of sites of transcription-factor binding and chromatin modification. Using two deeply sequenced data sets for human RNA polymerase II and STAT1, each with matching input-DNA controls, we describe a general scoring approach to address unique challenges in ChIP-seq data analysis.
0
0
0
465
490
1
Kanai A, Suzuki K, Tanimoto K, Mizushima-Sugano J, Suzuki Y, Sugano S. Characterization of STAT6 target genes in human B cells and lung epithelial cells. DNA Res. 2011;18(5):379-92.Using ChIP Seq, we identified 556 and 467 putative STAT6 target sites in the Burkitt's lymphoma cell line Ramos and in the normal lung epithelial cell line BEAS2B, respectively.
556
502
1
Kanai A, Suzuki K, Tanimoto K, Mizushima-Sugano J, Suzuki Y, Sugano S. Characterization of STAT6 target genes in human B cells and lung epithelial cells. DNA Res. 2011;18(5):379-92.Using ChIP Seq, we identified 556 and 467 putative STAT6 target sites in the Burkitt's lymphoma cell line Ramos and in the normal lung epithelial cell line BEAS2B, respectively.
6,383
2,394
1
Polycomb Repressive Complex 2 (PRC2) regulates key developmental genes in embryonic stem (ES) cells and during development. Here we show that Jarid2/Jumonji, a protein enriched in pluripotent cells and a founding member of the Jumonji C (JmjC) domain protein family, is a PRC2 subunit in ES cells. Genome-wide ChIP-seq analyses of Jarid2, Ezh2, and Suz12 binding reveal that Jarid2 and PRC2 occupy the same genomic regions. We further show that Jarid2 promotes PRC2 recruitment to the target genes while inhibiting PRC2 histone methyltransferase activity, suggesting that it acts as a "molecular rheostat" that finely calibrates PRC2 functions at developmental genes. Using Xenopus laevis as a model we demonstrate that Jarid2 knockdown impairs the induction of gastrulation genes in blastula embryos and results in failure of differentiation. Our findings illuminate a mechanism of histone methylation regulation in pluripotent cells and during early cell-fate transitions.
67
67
1
TAL1 (C)
pmid: 21241896
5,478
3,723
1
Hu G, Schones DE, Cui K, Ybarra R et al. Regulation of nucleosome landscape and transcription factor targeting at tissue-specific enhancers by BRG1. Genome Res 2011 Oct;21(10):1650-8. we identify GATA1-bound distal sites genome-wide and find a global reorganization of the nucleosomes at these potential enhancers during differentiation of hematopoietic stem cells (HSCs) to erythrocytes. We show that the catalytic subunit BRG1 of BAF complexes localizes to these distal sites during differentiation and generates a longer nucleosome linker region surrounding the GATA1 sites by shifting the flanking nucleosomes away.Intriguingly, we find that the nucleosome shifting specifically facilitates binding of TAL1 but not GATA1 and is linked to subsequent transcriptional regulation of target genes.
1,338
1,242
1
Induced pluripotent stem (iPS) cells can be obtained by the introduction of defined factors into somatic cells. The combination of Oct4 (also known as Pou5f1), Sox2 and Klf4 (which we term OSK) constitutes the minimal requirement for generating iPS cells from mouse embryonic fibroblasts. These cells are thought to resemble embryonic stem cells (ESCs) on the basis of global gene expression analyses; however, few studies have tested the ability and efficiency of iPS cells to contribute to chimaerism, colonization of germ tissues, and most importantly, germ-line transmission and live birth from iPS cells produced by tetraploid complementation. Using genomic analyses of ESC genes that have roles in pluripotency and fusion-mediated somatic cell reprogramming, here we show that the transcription factor Tbx3 significantly improves the quality of iPS cells. iPS cells generated with OSK and Tbx3 (OSKT) are superior in both germ-cell contribution to the gonads and germ-line transmission frequency. However, global gene expression profiling could not distinguish between OSK and OSKT iPS cells. Genome-wide chromatin immunoprecipitation sequencing analysis of Tbx3-binding sites in ESCs suggests that Tbx3 regulates pluripotency-associated and reprogramming factors, in addition to sharing many common downstream regulatory targets with Oct4, Sox2, Nanog and Smad1. This study underscores the intrinsic qualitative differences between iPS cells generated by different methods, and highlights the need to rigorously characterize iPS cells beyond in vitro studies.
517
209
123
TFe (C)
The goal of the TFe (Transcription Factor Encyclopedia) project is to create an online encyclopedic collection of well-studied transcription factor proteins, combining a mixture of both hand-curated and automatically-generated content to provide users with a wide set of information relevant to a transcription factor protein of their interest. http://www.cisreg.ca/cgi-bin/tfe/home.pl
14,548
7,806
1
TRIM24 (C)
pmid: 21164480
6,859
3,961
1
TRIM28 ChIP-chip dataset. Complete genomic analysis of KAP1 binding using a 38-array tiling set, identifying ~7,000 KAP1 binding sites. O'Geen H, Squazzo SL, Iyengar S, Blahnik K, Rinn JL, Chang HY, Green R, Farnham PJ. (2007) Genome-wide analysis of KAP1 binding suggests autoregulation of KRAB-ZNFs. PLoS Genet. 3(6):e89.
1,820
1,434
1
20
0
1
The Wasserman Lab Set is a special collection of binding sequences for selected sequences.
5,271
3,439
1
We performed genome-wide ChIP-seq for ZNF263, a C2H2 ZNF that contains 9 finger domains, a KRAB repression domain, and a SCAN domain and identified more than 5000 binding sites in K562 cells. Our results suggest that ZNF263 binds to a 24-nt site that differs from the motif predicted by the zinc finger code in several positions. Interestingly, many of the ZNF263 binding sites are located within the transcribed region of the target gene. Although ZNFs containing a KRAB domain are thought to function mainly as transcriptional repressors, many of the ZNF263 target genes are expressed at high levels. To address the biological role of ZNF263, we identified genes whose expression was altered by treatment of cells with ZNF263-specific small interfering RNAs. Our results suggest that ZNF263 can have both positive and negative effects on transcriptional regulation of its target genes.

Transcription factor binding profiles can be generated dynamically in this project.
(C)Project contains ChIP or ChIP-Seq data
 
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