Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RAC1 is an essential cofactor for estrogen receptor alpha [RNA-seq 1]

ABSTRACT: We identified a small GTPase protein RAC1 as an intrinsic cofactor in the estrogen receptor alpha (ER) complex that is required for the function of ER.

ORGANISM(S): Homo sapiens

PROVIDER: GSE169079 | GEO | 2021/08/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RAC1 is an essential cofactor for estrogen receptor alpha [ChIP-seq]

Project description:We identified a small GTPase protein RAC1 as an intrinsic cofactor in the estrogen receptor alpha (ER) complex that is required for the function of ER.

2021-08-09 | GSE169073 | GEO

RAC1 is an essential cofactor for estrogen receptor alpha [RNA-seq 2]

Project description:We identified a small GTPase protein RAC1 as an intrinsic cofactor in the estrogen receptor alpha (ER) complex that is required for the function of ER.

2021-08-09 | GSE169091 | GEO

RAC1 is an essential cofactor for estrogen receptor alpha

Project description:RAC1 is an essential cofactor for estrogen receptor alpha

| PRJNA715202 | ENA

RAC1 is an essential cofactor for estrogen receptor alpha [ChIP-seq]

Project description:RAC1 is an essential cofactor for estrogen receptor alpha [ChIP-seq]

| PRJNA715164 | ENA

RAC1 is an essential cofactor for estrogen receptor alpha [RNA-seq 2]

Project description:RAC1 is an essential cofactor for estrogen receptor alpha [RNA-seq 2]

| PRJNA715200 | ENA

RAC1 is an essential cofactor for estrogen receptor alpha [RNA-seq 1]

Project description:RAC1 is an essential cofactor for estrogen receptor alpha [RNA-seq 1]

| PRJNA715180 | ENA

RAC1 is an essential cofactor for estrogen receptor alpha

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-09 | GSE169096 | GEO

Cooperative interaction between retinoic acid receptor-alpha and estrogen receptor in breast cancer.

Project description:Retinoic acid receptor-alpha (RAR alpha) is a known estrogen target gene in breast cancer cells. The consequence of RAR alpha induction by estrogen was previously unknown. We now show that RAR alpha is required for efficient estrogen receptor-alpha (ER)-mediated transcription and cell proliferation. RAR alpha can interact with ER-binding sites, but this occurs in an ER-dependent manner, providing a novel role for RAR alpha that is independent of its classic role. We show, on a genome-wide scale, that RAR alpha and ER can co-occupy regulatory regions together within the chromatin. This transcriptionally active co-occupancy and dependency occurs when exposed to the predominant breast cancer hormone, estrogen--an interaction that is promoted by the estrogen-ER induction of RAR alpha. These findings implicate RAR alpha as an essential component of the ER complex, potentially by maintaining ER-cofactor interactions, and suggest that different nuclear receptors can cooperate for effective transcriptional activity in breast cancer cells. RAR alpha silenced breast cancer MCF-7 cell lines or control siRNA in the presence of estrogen or a vehicle. MCF-7 cells were hormone-depleted for 3 d and treated with 100 nM estrogen for 12 h. There were three biological replicates for each of the four different groups.

2010-06-16 | E-GEOD-22213 | biostudies-arrayexpress

Cooperative interaction between retinoic acid receptor-alpha and estrogen receptor in breast cancer.

2010-06-09 | GSE22213 | GEO

Neurofibromin is an Estrogen Receptor alpha Transcriptional Co-repressor in Breast cancer

Project description:We report that neurofibromin, a tumor suppressor and Ras-GAP (GTPase Activating Protein), is also an estrogen receptor-alpha (ER) transcriptional co-repressor through leucine/isoleucine-rich motifs that are functionally independent of GAP activity. GAP activity, in turn, does not impact ER binding. Consequently, neurofibromin-depletion causes estradiol hypersensitivity and tamoxifen agonism, explaining the poor prognosis associated with neurofibromin-loss in endocrine therapy-treated ER+ breast cancer. Neurofibromin-deficient ER+ breast cancer cells initially retain sensitivity to selective estrogen receptor degraders (SERDs). However, Ras activation does play a role in acquired SERD resistance, which can be reversed upon MEK inhibitor addition, and SERD/MEK inhibitor combinations induce tumor regression. Thus, neurofibromin is a dual repressor for both Ras and ER signaling, and co-targeting may treat neurofibromin-deficient ER+ breast tumors.

2020-02-14 | GSE142479 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data