Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Response to estradiol-ERalpha

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE9757 | GEO | 2007/12/04

SECONDARY ACCESSION(S): PRJNA105105

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Response to estradiol-ERalpha ERE Binding defective mutant

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

Transcription profiling of human cell response to estradiol-ERalpha

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

Transcription profiling of human cells transfected with the recombinant adenovirus bearing no cDNA (CMV) or cDNA for ERalpha 203/204/211E (3411E) for 48h

2008-06-16 | E-GEOD-9758 | biostudies-arrayexpress

Response to estradiol-ERbeta and estradiol-ERbeta ERE binding defective mutant

Project description:In addition to the estrogen responsive element (ERE)-dependent gene expression, E2-ERbeta 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-ERbeta signaling is unclear. Our studies in infected ER-negative cell models with an ERbeta mutant (ERbetaDBD) that functions exclusively at the ERE-independent pathway demonstrated that genomic responses assessed by microarrays from the ERE-independent pathway to E2-ERbeta are not sufficient to alter cellular growth, death or motility. These findings suggest that the ERE-dependent pathway is the canonical E2-ERbeta signaling in model cell lines. Keywords: MDA-MB-231 cells

2007-12-04 | GSE9759 | GEO

Transcription profiling of human ER negative cells response to estradiol-ERbeta and estradiol-ERbeta ERE binding defective mutant

2008-06-16 | E-GEOD-9759 | biostudies-arrayexpress

Transcription profiling of human breast cancer cells expressing ERalpha and treated with 17beta-estradiol

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 0Â·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.

2007-08-25 | E-GEOD-2251 | biostudies-arrayexpress

Transcription profiling of human MDA-MB-231 cells response to adenovirus expressed estradiol-ERalpha, estradiol-Erbeta, and ERE Binding defective mutants

Project description:This SuperSeries is composed of the following subset Series:; GSE9757: Response to estradiol-ERalpha; GSE9758: Response to estradiol-ERalpha ERE Binding defective mutant; GSE9759: Response to estradiol-Erbeta and estradiol-ERbeta ERE binding defective mutant Experiment Overall Design: Refer to individual Series

2008-06-16 | E-GEOD-9761 | biostudies-arrayexpress

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.

2009-03-09 | GSE14664 | GEO

Anti-prolif. effect of E2 in breast cancer cells that re-exp. ERalpha is mediated by aberr. regulat. of cell cycle genes

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

2005-02-09 | GSE2251 | GEO

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

2009-03-09 | E-GEOD-14664 | biostudies-arrayexpress