E-MTAB-10328
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-10328 | ExpressionAtlas | 2025-07-07
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-10328-analysis-methods.tsv | Tabular | |||
| E-MTAB-10328-analytics.tsv | Tabular | |||
| E-MTAB-10328-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-10328-configuration.xml | Xml | |||
| E-MTAB-10328-g4_g1-mvaPlot.png | Other |
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Project description:Transcription factor recruitment to genomic sites of action is primarily due to direct protein:DNA interactions. The subsequent recruitment of co-regulatory complexes leads to either transcriptional activation or repression. In contrast to this canonical scheme, some transcription factors such as the glucocorticoid receptor (GR) behave as transcriptional repressors when recruited to target genes through protein tethering. We have investigated the genome-wide prevalence of tethering between GR and Stat3 and found non-reciprocal interactions, namely that GR tethering to DNA-bound Stat3 results in transcriptional repression whereas Stat3 tethering to GR results in synergism. Further, other schemes of GR and Stat3 co-recruitment to regulatory modules result in transcriptional synergism, including neighbouring and composite binding sites. The results indicate extensive transcriptional interactions between Stat3 and GR; further, they provide a genome-wide assessment of transcriptional regulation by tethering and a molecular basis for integration of signals mediated by GR and Stats in health and disease. ChIP-seq analysis of Stat3 and GR binding sites in pituitary corticotroph AtT-20 cell model. Five independant ChIPs were pooled prior library preparation for each contitions: STAT3 (LIF), STAT3 (Dex+LIF), GR (Dex+LIF), GR (Dex) and control IgG.
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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. 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
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2014-03-12 | E-GEOD-55810 | biostudies-arrayexpress
Project description:Pathogen-associated molecular patterns such as lipopolysaccharide (LPS) mimic immune responses triggered by bacterial infections. The hormonally active form of vitamin D, 1α,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃], supports innate immunity, but its molecular mechanisms remain incompletely understood. Here, we investigated epigenomic and transcriptomic changes in THP-1 monocytes exposed to 1,25(OH)₂D₃, LPS, or their combination over 24–48 hours. Epigenome profiling via ATAC-seq revealed that co-stimulation with 1,25(OH)₂D₃ and LPS induces substantially more chromatin accessibility changes than either treatment alone, with up to 81% of altered regions uniquely responsive to the combination. Motif enrichment analysis highlighted JUN/FOS transcription factors as key regulators of this synergistic response. Transcriptomic analysis via RNA-seq mirrored these findings, though fewer genes than chromatin regions were affected. Notably, under 1,25(OH)₂D₃-primed conditions, 333 genes exhibited synergistic expression changes upon co-treatment, meaning their responses significantly deviates from the additive effects of the individual stimulations. This includes 267 previously unrecognized as vitamin D targets. Functional annotation revealed these genes are primarily linked to monocyte and T cell differentiation, in contrast to classical vitamin D targets associated with inflammation. In conclusion, our findings uncover a distinct and cooperative regulatory program driven by vitamin D and LPS, advancing our understanding of how vitamin D shapes immune responses at the chromatin and transcriptional levels.
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Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Here, we reveal a novel cistromic circuit in HSCs comprising the vitamin D receptor (VDR) and SMAD transcription factors that restrains the intensity of hepatic fibrogenesis. Ligand-activated VDR suppresses TGFβ1-induced pro-fibrotic gene expression in HSCs. Administration of a vitamin D analogue, calcipotriol, diminishes the fibrotic response in a mouse model of liver fibrosis, while VDR knockout mice spontaneous develop extensive hepatic fibrosis by age 6 months. Using ChIP-Seq, we find that the anti-fibrotic properties of VDR are due to crosstalk with SMAD, mediated by their co-occupancy of DNA-binding sites on pro-fibrotic genes. Specifically, SMAD binding potentiates local chromatin accessibility to enhance VDR recruitment at the same cis-regulatory elements, which reciprocally antagonizes the interaction between SMAD3 and chromatin and limits the assembly of transcriptional activation complexes at fibrotic genes, a process that is enhanced by the presence of VDR agonists. These results not only establish this coordinated VDR/SMAD cistromic circuit as a master regulator of hepatic fibrogenesis, but also support VDR as a potential drug target to ameliorate liver fibrosis. Identification of VDR, SMAD3 and H3 binding sites in human stellate LX2 cells that were pre-treated with calcipotriol (100nM) for 16 hrs (where calcipotriol treatment is indicated) followed by incubation of calcipotriol (100nM) or TGFβ1 (1ng/ml) for another 4 hours (where indicated).
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Project description:Transcription factor recruitment to genomic sites of action is primarily due to direct protein:DNA interactions. The subsequent recruitment of co-regulatory complexes leads to either transcriptional activation or repression. In contrast to this canonical scheme, some transcription factors such as the glucocorticoid receptor (GR) behave as transcriptional repressors when recruited to target genes through protein tethering. We have investigated the genome-wide prevalence of tethering between GR and Stat3 and found non-reciprocal interactions, namely that GR tethering to DNA-bound Stat3 results in transcriptional repression whereas Stat3 tethering to GR results in synergism. Further, other schemes of GR and Stat3 co-recruitment to regulatory modules result in transcriptional synergism, including neighbouring and composite binding sites. The results indicate extensive transcriptional interactions between Stat3 and GR; further, they provide a genome-wide assessment of transcriptional regulation by tethering and a molecular basis for integration of signals mediated by GR and Stats in health and disease.
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The work (proposal:https://doi.org/10.46936/10.25585/60001318) conducted by the U.S. Department of Energy Joint Genome Institute (https://ror.org/04xm1d337), a DOE Office of Science User Facility, is supported by the Office of Science of the U.S. Department of Energy operated under Contract No. DE-AC02-05CH11231.
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