Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA149499 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine the role of estrogen-related receptor alpha and gamma (ERRa/g) on chromatin accessibility, we performed ATAC-seq studies with WT control and ERRa/g KO hiPSC-CMs. We found that ERRa/g activates cardiac chromatin accessibilities in hiPSC-CMs. A subset of the decreased ATAC signals by loss of ERRa/g overlapped ERRg peaks (GSE113760) in hiPSC-CMs, suggesting that ERRg might be directly involved in the activation of cardiac chromatin accessibilities. The motif analysis with decreased ATAC signal by loss of ERRa/g revealed that cardiac-enriched transcription factors such as MEF2 and GATA could cooperate with ERR.
2022-02-16 | GSE165962 | GEO
Project description:ERRa is an orphan nuclear receptor with an established role in cell metabolism. Our studies demonstrate that acute or chronic loss of ERRa broadly affects mitochondrial and glycolytic metabolism in CD4+ T cells and results in diminished T cell function and differentation. In this array, we assessed the contribution of ERRa to changes in gene expression in resting and stimulated CD4+ T cells with the goal of identifying specific metabolic genes that exhibit altered expression in the presence or absence of ERRa. Please see related publication: Michalek, et al. PNAS 2011.
2011-10-21 | GSE33108 | GEO
Project description:Role of Estrogen Receptor α in Mouse Oviduct Gene Expression
| PRJNA160171 | ENA
Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
2019-11-12 | PXD007511 | Pride
Project description:ERRa is an orphan nuclear receptor with an established role in cell metabolism. Our studies demonstrate that acute or chronic loss of ERRa broadly affects mitochondrial and glycolytic metabolism in CD4+ T cells and results in diminished T cell function and differentation. In this array, we assessed the contribution of ERRa to changes in gene expression in resting and stimulated CD4+ T cells with the goal of identifying specific metabolic genes that exhibit altered expression in the presence or absence of ERRa. Please see related publication: Michalek, et al. PNAS 2011. CD4+ T cells from 6-8 week old mice were negatively selected (Miltenyi), resulting in >95% purity and cultured in RPMI 1640 (Mediatech) with 10% FBS (Gemini Bio-Products). Wild-type (WT) and ERRa−/− (ERRKO) CD4+ T cells were harvested directly ex vivo or stimulated with anti-CD3 and anti-CD28 antibodies for 12 h in the presence or absence of the pharmacological inhibtors of ERRa XCT790 and Compound A. RNA was harvested using the RNeasy Plus kit from Qiagen.The microarray was prepared and analyzed by the Duke Microarray Facility using Ambion Message Amp Premier labeling and Affymetrix GeneChip Mouse Genome 430A 2.0. Each assay contains three independent biologic replicates.
2011-10-20 | E-GEOD-33108 | biostudies-arrayexpress
Project description:This dataset is part of the manuscript titled "The metabolic regulator ERRalpha, a downstream target of HER2/IGF1, as a therapeutic target in breast cancer" (in review). The expression data obtained in human mammary epithelial cells were used to generate a list of ERRalpha-regulated genes that was later refined in clinical breast cancer datasets to generate a clinically relevant signature of ERalpha activity (referred to as Cluster 3 signature). Using this signature of the estrogen-related receptor alpha (ERRa) to profile more than eight-hundred breast tumors, we found that patients with tumors exhibiting higher ERRa activity were predicted to have shorter disease free survival. Further, the ability of an ERRa antagonist, XCT790, to inhibit breast cancer cell proliferation correlates with the cell’s intrinsic ERRa activity. These findings highlight the potential of using the ERRa signature and antagonists in targeted therapy for breast cancer. Using a chemical genomic approach we determined that activation of the HER2/IGF1 signaling pathways upregulates the expression of PGC-1b, an obligate cofactor for ERRa activity. Knockdown of PGC-1b in HER2 positive breast cancer cells impaired ERRa signaling and reduced cell proliferation, implicating a functional role of PGC1b/ERRa in the pathogenesis HER2 positive breast cancer.
2010-11-01 | GSE23061 | GEO
Project description:Transcriptional regulatory circuits that drive cardiomyocyte maturation during the developmental process are poorly understood. Estrogen-related receptor alpha and gamma (ERRa/g) have been shown to be involved in all aspects of mitochondrial energy production. However, the function of ERR during the postnatal cardiac developmental process is unclear. To examine the role of (ERRa/g) during postnatal cardiac maturation, we generated inducible cardiac-specific ERRa/g knockdown (KD) mice with adeno-associated virus serotype 9 (AAV9) expressing Cre. We found that at P35 a number of genes involved in oxidative mitochondrial metabolism including OXPHOS, TCA cycle, branched chain amino acid catabolism, and fatty acid oxidation were dramatically downregulated. Also, the KD hearts exhibited a significant downregulation of adult cardiac contractile protein, ion channel and Ca2+ handling genes. In contrast, fetal cardiac genes and non-cardiac genes that express in fibroblast or skeletal muscle cells were ectopically induced in the KD hearts. These results suggest that ERRa/g are essential factors for the broad postnatal cardiomyocyte maturation program.
2020-06-10 | GSE135347 | GEO
Project description:Transcriptional regulatory circuits that drive cardiomyocyte maturation during the developmental process are poorly understood. Estrogen-related receptor alpha and gamma (ERRa/g) have been shown to be involved in all aspects of mitochondrial energy production. However, the function of ERR during the cardiac developmental process is not understood well. To examine the role of (ERRa/g), we generated cardiac-specific ERRa/g knockout (KO) mice and found that the KO mice died within 24 hours post-birth. At embryonic age 17.5, a number of genes involved in oxidative mitochondrial metabolism including OXPHOS, TCA cycle, and fatty acid oxidation were dramatically downregulated. Also, the mutant hearts exhibited a significant downregulation of adult cardiac contractile protein, ion channel and Ca2+ handling genes. In contrast, fetal cardiac genes and non-cardiac genes that express in fibroblast or endothelial cells were ectopically induced in the KO hearts. These results suggest that ERRa/g are essential factors for the broad cardiomyocyte maturation program.
2020-06-10 | GSE113761 | GEO
Project description:Orphan nuclear receptor estrogen-related receptor alpha (ERRα) has recently been shown to carry negative prognostic significance in breast and ovarian cancers. The specific role of ERRα in tumor growth and progression, however, is yet to be fully understood. The significant homology between estrogen receptor alpha (ERα) and ERRα initially suggested that these receptors may share similar transcriptional targets. Using the well-characterized ERα-positive MCF-7 breast cancer cell line, we sought to gain a genome-wide picture of ERα-ERRα cross-talk using an unbiased microarray approach. Since a small molecule ligand has not been identified for ERRα, its transcriptional activity in these studies was induced using its known coactivator PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1α) as a protein ligand. Both wild-type PGC1, as well as ERRa-specific variant (PGC1 2x9) were used to activate ERRa. Non-NR-dependent activities of PGC-1α were controlled for using a variant PGC-1α in which the leucines within the NR-interacting domain had been mutated to alanines (L2L3M). Beta-galactosidase (BGAL) overexpression was used as a non-specific background control. Activation of endogenous ER was achieved by treatment with 10 nM estadiol. Keywords: Response to stimulus
2008-08-25 | GSE11266 | GEO
Project description:Orphan nuclear receptor estrogen-related receptor alpha (ERRα) has recently been shown to carry negative prognostic significance in breast and ovarian cancers. The specific role of ERRα in tumor growth and progression, however, is yet to be fully understood. The significant homology between estrogen receptor alpha (ERα) and ERRα initially suggested that these receptors may share similar transcriptional targets. Using the well-characterized ERα-positive MCF-7 breast cancer cell line, we sought to gain a genome-wide picture of ERα-ERRα cross-talk using an unbiased microarray approach. Since a small molecule ligand has not been identified for ERRα, its transcriptional activity in these studies was induced using its known coactivator PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1α) as a protein ligand. Both wild-type PGC1, as well as ERRa-specific variant (PGC1 2x9) were used to activate ERRa. Non-NR-dependent activities of PGC-1α were controlled for using a variant PGC-1α in which the leucines within the NR-interacting domain had been mutated to alanines (L2L3M). Beta-galactosidase (BGAL) overexpression was used as a non-specific background control. Activation of endogenous ER was achieved by treatment with 10 nM estadiol. Experiment Overall Design: MCF7 cells were infected with adenovirus overexpressing one of the four proteins (PGC1 WT, PGC1 2x9, PGC1 L2L3 and BGAL); Twelve hours post infection cells were then treated with either 10 nM estradiol (E2)or ethanol vehicle for 12 hours. Each combination of infection and treatment was was repeated three times in three independent experiments. A total of 23 samples are presented. Two replicates instead of three are shown for PGC1 WT E2 for technical reasons.
2008-10-25 | E-GEOD-11266 | biostudies-arrayexpress