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ERalpha ChIP-chip from HeLA-ER cells treated with E2

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22099 | GEO | 2011/02/22

SECONDARY ACCESSION(S): PRJNA128919

REPOSITORIES: GEO

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ERalpha ChIP-chip from HeLA-ER cells treated with E2

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

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Project description:ChIP followed by deep sequencing was performed with antibodies to ERalpha in U2OS-ERalpha cells treated with 17beta-estradiol.

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Project description:Gene expression changes caused by estrogen treatment of breast cancer cells that re-express ERalpha was investigated by infecting ER-negative MDA-MB-231 breast cancer cells for 24 h with recombinant adenovirus encoding full-length human ERalpha (Ad-ERalpha) or control vector (Ad-LacZ), and treating them with 0·01% ethanol (vehicle control) or 10-8 M 17beta-estradiol (E2). After 48 h of treatment, total RNA was isolated and used for transcript profiling on Affymetrix GeneChips. Three independent biological replicates of this experiment were carried out. Keywords: ordered

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Estrogen signaling and the Metabolic Syndrome: Targeting the hepatic ERalpha action

Project description:We have previously shown that total estrogen receptor alpha (ERalpha knockout (KO) mice exhibit hepatic insulin resistance. To investigate the contribution of hepatic ERalpha action for the observed phenotype, we established a liver-selective ERalphaKO mouse model, LERKO. We demonstrate that LERKO mice have efficient reduction of ERalpha selectively within the liver. However, LERKO and wild type control mice do not differ in body weight, and have a comparable hormone profile as well as insulin and glucose response, even when challenged with a high fat diet. Furthermore, LERKO mice display very minor changes in their hepatic transcript profile. Collectively, our findings indicate that hepatic ERalpha action may not be the initiating factor for the previously identified hepatic insulin resistance in ERalphaKO mice.

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ChIP-Seq of ERalpha and RNA polymerase II defines genes differentially responding to ligands

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.

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Response to estradiol-ERalpha ERE Binding defective mutant

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