Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA128919 | ENA |
REPOSITORIES: ENA
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Project description:We are studying the mechanisms by which the estrogen receptor, ERalpha, is recruited to and regulates genes with a non-direct DNA binding. We performed ChIP-chip for ERalpha in E2 treated HeLa-ER cells, and looked at 19000 RefSeq genes to determine binding patterns of the receptor at promoters. The experiment was performed in duplicate. ChIP-chip biological replicates for Eralpha in E2 treated HeLa-ER cells are included.
2011-02-22 | E-GEOD-22099 | biostudies-arrayexpress
Project description:We are studying the mechanisms by which the estrogen receptor, ERalpha, is recruited to and regulates genes with a non-direct DNA binding. We performed ChIP-chip for ERalpha in E2 treated HeLa-ER cells, and looked at 19000 RefSeq genes to determine binding patterns of the receptor at promoters. The experiment was performed in duplicate.
2011-02-22 | GSE22099 | GEO
Project description:In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERalpha regulates transcription through functional interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. Our studies in infected ER-negative cell models with an ERalpha mutant (ERalpha 203/204/211E) that functions exclusively at the ERE-independent pathway demonstrated that genomic responses assessed by microarrays from the ERE-independent pathway to E2-ERalpha are not sufficient to alter cellular growth, death or motility. These findings suggest that the ERE-dependent pathway is the canonical E2-ERalpha signaling in model cell lines. Keywords: MDA-MB-231 cells
2007-12-04 | GSE9758 | GEO
Project description:In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERalpha regulates transcription through functional interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. Our studies in infected ER-negative cell models with an ERalpha mutant (ERalpha 203/204/211E) that functions exclusively at the ERE-independent pathway demonstrated that genomic responses assessed by microarrays from the ERE-independent pathway to E2-ERalpha are not sufficient to alter cellular growth, death or motility. These findings suggest that the ERE-dependent pathway is the canonical E2-ERalpha signaling in model cell lines. Experiment Overall Design: Cells were infected with the recombinant adenovirus bearing no cDNA (CMV) or cDNA for ERalpha 203/204/211E (3411E) for 48h. Infected cells were then treated with 1 nM Estradiol 17beta for 6h. All experiments were repeated six independent times conducted at at six different days
2008-06-16 | E-GEOD-9758 | biostudies-arrayexpress
Project description:In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERalpha regulates transcription through functional interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. Our studies in infected ER-negative cell models with an ERalpha demonstrated that genomic responses assessed by microarrays from the alter cellular growth, death or motility. Keywords: MDA-MB-231 cells
2007-12-04 | GSE9757 | GEO
Project description:We used ChIP-Seq to map ERalpha binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identified 10,205 high confidence ERalpha binding sites in response to E2 of which 68% contained an estrogen response element (ERE) and only 7% contained a FOXA1 motif. Remarkably, 596 genes already change significantly in RNAPII occupancy (59% up and 41% down) following one hour of E2 exposure. Although pausing of RNA polymerase II occurs frequently in MCF-7 cells (17%) it is only observed on a minority of E2-regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERalpha DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both antagonists act differently on E2-downregulated genes. Tamoxifen acts as an agonist, also downregulating these genes while fulvestrant antagonizes E2 induced repression and often increases RNAPII occupancy. Furthermore our data identified genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus, antagonist loaded ERalpha acts mechanistically different on E2-activated and E2-repressed genes.
2009-03-09 | GSE14664 | GEO
Project description:In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERalpha regulates transcription through functional interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. Our studies in infected ER-negative cell models with an ERalpha demonstrated that genomic responses assessed by microarrays from the alter cellular growth, death or motility. Experiment Overall Design: Cells were infected with the recombinant adenovirus bearing no cDNA (CMV) or cDNA for ERalpha for 48h. Infected cells were then treated with 1 nM Estradiol 17beta for 6h. All experiments were repeated six independent times conducted at at six different days
2008-06-16 | E-GEOD-9757 | biostudies-arrayexpress
Project description:To explore the global mechanisms of estrogen-regulated transcription, we used chromatin immunoprecipitation coupled with DNA microarrays to determine the localization of RNA polymerase II (Pol II), estrogen receptor alpha (ERalpha), steroid receptor coactivator proteins (SRC), and acetylated histones H3/H4 (AcH) at estrogen-regulated promoters in MCF-7 cells with or without estradiol (E2) treatment. In addition, we correlated factor occupancy with gene expression and the presence of transcription factor binding elements. Using this integrative approach, we defined a set of 58 direct E2 target genes based on E2-regulated Pol II occupancy and classified their promoters based on factor binding, histone modification, and transcriptional output. Many of these direct E2 target genes exhibit interesting modes of regulation and biological activities, some of which may be relevant to the onset and proliferation of breast cancers. Our studies indicate that about one-third of these direct E2 target genes contain promoter-proximal ERalpha-binding sites, which is considerably more than previous estimates. Some of these genes represent possible novel targets for regulation through the ERalpha/AP-1 tethering pathway. Our studies have also revealed several previously uncharacterized global features of E2-regulated gene expression, including strong positive correlations between Pol II occupancy and AcH levels, as well as between the E2-dependent recruitment of ERalpha and SRC at the promoters of E2-stimulated genes. Furthermore, our studies have revealed new mechanistic insights into E2-regulated gene expression, including the absence of SRC binding at E2-repressed genes and the presence of constitutively bound, promoter-proximally paused Pol IIs at some E2-regulated promoters. These mechanistic insights are likely to be relevant for understanding gene regulation by a wide variety of nuclear receptors. Keywords: MCF7 cells, E2, Estrogen, RNA, ER, RNA Polymerase II, SRC, Acetylated histones, ChIP-chip
2007-10-19 | GSE9253 | GEO
Project description:We used ChIP-Seq to map ERalpha binding sites and to profile changes in RNA polymerase II (RNAPII) occupancy in MCF-7 cells in response to estradiol (E2), tamoxifen or fulvestrant. We identified 10,205 high confidence ERalpha binding sites in response to E2 of which 68% contained an estrogen response element (ERE) and only 7% contained a FOXA1 motif. Remarkably, 596 genes already change significantly in RNAPII occupancy (59% up and 41% down) following one hour of E2 exposure. Although pausing of RNA polymerase II occurs frequently in MCF-7 cells (17%) it is only observed on a minority of E2-regulated genes (4%). Tamoxifen and fulvestrant partially reduce ERalpha DNA binding and prevent RNAPII loading on the promoter and coding body on E2-upregulated genes. Both antagonists act differently on E2-downregulated genes. Tamoxifen acts as an agonist, also downregulating these genes while fulvestrant antagonizes E2 induced repression and often increases RNAPII occupancy. Furthermore our data identified genes preferentially regulated by tamoxifen but not by E2 or fulvestrant. Thus, antagonist loaded ERalpha acts mechanistically different on E2-activated and E2-repressed genes. Examination of ERalpha binding sites upon the binding of different ligands and association with transcription via RNAPII occupancy.
2009-03-09 | E-GEOD-14664 | biostudies-arrayexpress
Project description:Abstract: Inhibitory crosstalk between estrogen receptor alpha (ERalpha) and aryl hydrocarbon receptor (AHR) regulates 17β-estradiol (E2)-dependent breast cancer cell signalling. ERalpha and AHR are transcription factors activated by E2 and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) respectively. Dietary ligands resveratrol (RES) and 3,3´diindolylmethane (DIM) also activate ERalpha while only DIM activates AHR and RES represses it. DIM and RES are reported to have anti-cancer and anti-inflammatory properties. Studies with genome wide targets and AHR and ERalpha regulated genes after DIM and RES are unknown. We used chromatin immunoprecipitation with high-throughput sequencing and transcriptomics to study ERalpha as well as AHR coregulation in MCF-7 human breast cancer cells treated with DIM, RES, E2 or TCDD alone or E2+TCDD for 1 and 6 hours respectively. ERalpha bound sites after DIM enriched for the AHR motif but not after E2 or RES while AHR bound sites after DIM and E2+TCDD enriched for the ERE motif but not after TCDD. More than 90% of the differentially expressed genes closest to an AHR binding site after DIM or E2+TCDD also had an ERalpha site and 60% of coregulated genes between DIM and E2+TCDD were common. Collectively our data shows that RES and DIM differentially regulate multiple transcriptomic targets via ERalpha and ERalpha/AHR coactivity respectively, which need to be considered to properly interpret their cellular and biological responses. These novel data also suggest that when both receptors are activated, ERalpha dominates with preferential recruitment of AHR to ERalpha target genes.
2023-10-16 | GSE232233 | GEO