Homo sapiens
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PROVIDER: PRJNA135845 | ENA |
REPOSITORIES: ENA
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Project description:In each cell type the expression of genes is regulated by the action of a large number of transcription factors, but so far we have only a rudimentary knowledge of the location of the gene regulatory elements where they bind. This can now be addressed with genome-wide ChIP experiments. In a previous ChIP-chip study of USF1 and USF2 we found evidence also of binding of GABP, FOXA2 and HNF4a within the enriched regions. Here we have applied ChIP-seq for these transcription factors and identified 3064 peaks of enrichment for GABP, 7266 for FOXA2 and 18783 for HNF4a. HNF4a and FOXA2 binding was found in at least half of the regions previously identified as bound by USF2 but not USF1, showing that they frequently bind the same regulatory elements. GABP peaks were found at transcription start sites whereas 94 % of FOXA2 and 90 % of HNF4a peaks were located at other positions. We developed a method based on the high resolution achieved by ChIP-seq to accurately define TFBS within peaks, and found the predicted sites to have an elevated conservation level compared to peak centers; however the majority of bindings were not evolutionary conserved. An unexpected interaction between HNF4a and GABP was seen at TSS, with as many as 1/3 of the HNF4a positive promoters being bound also by GABP, and co-immunoprecipitations show that these factors are in the same complex in the nucleus.
2009-06-09 | E-MTAB-115 | biostudies-arrayexpress
Project description:In each cell type the expression of genes is regulated by the action of a large number of transcription factors, but so far we have only a rudimentary knowledge of the location of the gene regulatory elements where they bind. This can now be addressed with genome-wide ChIP experiments. In a previous ChIP-chip study of USF1 and USF2 we found evidence also of binding of GABP, FOXA2 and HNF4a within the enriched regions. Here we have applied ChIP-seq for these transcription factors and identified 3064 peaks of enrichment for GABP, 7266 for FOXA2 and 18783 for HNF4a. HNF4a and FOXA2 binding was found in at least half of the regions previously identified as bound by USF2 but not USF1, showing that they frequently bind the same regulatory elements. GABP peaks were found at transcription start sites whereas 94 % of FOXA2 and 90 % of HNF4a peaks were located at other positions. We developed a method based on the high resolution achieved by ChIP-seq to accurately define TFBS within peaks, and found the predicted sites to have an elevated conservation level compared to peak centers; however the majority of bindings were not evolutionary conserved. An unexpected interaction between HNF4a and GABP was seen at TSS, with as many as 1/3 of the HNF4a positive promoters being bound also by GABP, and co-immunoprecipitations show that these factors are in the same complex in the nucleus. ArrayExpress Release Date: 2009-06-10 Publication Title: Molecular interactions between HNF4a, FOXA2 and GABP identified at regulatory DNA elements through ChIP-sequencing Publication Author List: Ola Wallerman, Mehdi Motallebipour, Stefan Enroth, Kalicharan Patra, MadhuSudan Reddy Bysani, Jan Komorowski, Claes Wadelius Person Roles: submitter Person Last Name: Wallerman Person First Name: Ola Person Mid Initials: Person Email: ola.wallerman@genpat.uu.se Person Phone: Person Address: IGP, Rudbecklab Person Affiliation: Uppsala University
2011-02-05 | GSE25694 | GEO
Project description:ChIP-seqs of BMAL1, HNF4A, FOXA2, H3K4me1, and H3K27ac were profiled in mouse liver tissues upon Hnf4a or Bmal1 knockout. BMAL1, H3K4me1, and H3K27ac ChIP-seq were profiled in U2OS cells ectopically expressing HNF4A.
2021-09-23 | GSE157452 | GEO
Project description:Hereditary Leiomyomatosis and renal cell cancer is caused by fumarate hydratase loss of heterozygosity and subsequence accumulation of fumarate. Fumarate is known to activate the anti-oxidant response and is key for cellular survival. Fumarate succinates KEAP1 which releases NRF2 to activate the antioxidant response. The role of fumarate on the global regulatory chromatin landscape is less understood. Here, by integrating chromatin accessibility and histone ChIP-seq profiles, we identify complex transcription factor networks involved in the highly remodelled chromatin landscape of FH-deficient cells. We implicate FOXA2 in the maintenance of FH-deficient cells by regulating anti-oxidant response genes and subsequent metabolic output, independent of NRF2. These results identify new redox and amino acid metabolism regulators and provide new avenues for therapeutic intervention.
2022-06-01 | ST002199 | MetabolomicsWorkbench
Project description:Specific regulation of target genes by transforming growth factor-β (TGF-β) in a given cellular context is determined in part by transcription factors and cofactors that interact with the Smad complex. In the present study, we determined Smad2 and Smad3 (Smad2/3) binding regions in the promoters of known genes in HepG2 hepatoblastoma cells, and compared them to those in HaCaT epidermal keratinocytes to elucidate the mechanisms of cell type- and context-dependent regulation of transcription induced by TGF-β. Our results show that 81% of the Smad2/3 binding regions in HepG2 cells were not shared with those found in HaCaT cells. Hepatocyte nuclear factor 4α (HNF4α) is expressed in HepG2 cells, but not in HaCaT cells, and the HNF4α binding motif was identified as an enriched motif in the HepG2-specific Smad2/3 binding regions. ChIP-sequencing analysis of HNF4A binding regions under TGF-β stimulation revealed that 32.5% of the Smad2/3 binding regions overlapped HNF4A bindings. MIXL1 was identified as a new combinatorial target of HNF4A and Smad2/3, and both the HNF4A protein and its binding motif were required for the induction of MIXL1 by TGF-β in HepG2 cells. These findings generalize the importance of binding of HNF4A on Smad2/3 binding genomic regions for HepG2-specific regulation of transcription by TGF-β, and suggest that certain transcription factors expressed in a cell-type-specific manner play important roles in the transcription regulated by the TGF-β-Smad signaling pathway. HepG2 cells were treated with TGF-beta for 1.5 h or left untreated. anti-HNF4A ChIP-seq was performed. One lane was used for each sample.
2011-06-08 | E-GEOD-28845 | biostudies-arrayexpress
Project description:ChIP-Seq analysis of HNF4A and FOXA2 in embryonic mouse liver
| PRJNA236762 | ENA
Project description:Smad2/3 are transcription factors that engage in TGF-beta-induced transcription. We determined and analyzed HepG2 and Hep3B-specific Smad2/3 binding sites by ChIP-chip. We used expression microarrays to compare the Smad2/3 and HNF4alpha binding sites identified by ChIP-chip or ChIP-seq, respectively, to TGF-beta-induced gene expressions. HepG2 cells were transfected with control or HNF4A siRNAs and treated with 3 ng/ml TGF-beta for 0, 1.5 and 24 h (6 samples in total, no replicates). Total RNA was extracted and expression microarray analysis was performed as described in the protocols.
2011-06-08 | E-GEOD-28590 | biostudies-arrayexpress
Project description:FOXA2 ChIP-seq on human HepG2 For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2017-10-20 | GSE105218 | GEO
Project description:We used ChIP-Seq to map GABP-alpha binding sites in human hematopoietic progenitor cells (HPCs). Coupled with functional assays using GABP-alpha deficient mouse model and bioinformatics analysis, we systematically determined a transcriptional module controlled by GABP in HPCs.
2010-12-10 | GSE24933 | GEO