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

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

PROVIDER: PRJNA715180 | ENA |

REPOSITORIES: ENA

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RAC1 is an essential cofactor for estrogen receptor alpha

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

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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.

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

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.

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

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

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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]

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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

Microglial Rac1 is essential for experience-dependent brain plasticity and cognitive performance

Project description:Microglia, the largest population of brain immune cells, continuously interact with synapses to maintain brain homeostasis. We aimed at understanding the role of Rac1 on microglia functions. Here, we used conditional cell-specific gene targeting in mice with multi-omics approaches, and demonstrated that the RhoGTPase Rac1 was an essential requirement for the microglia to sense and interpret the brain microenvironment, and for crucial microglia-synapse crosstalk driving experience-dependent plasticity, a fundamental brain property impaired in several neuropsychiatric disorders.

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