Role of Retinoids x Receptor in Mouse Liver
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Yuqi He
PROVIDER: E-GEOD-46762 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Genome-wide binding of Retinoids x Receptor and Retinoic Acid Receptor in mouse liver was described
2013-05-15 | GSE46762 | GEO
Project description:For the genome-wide analysis using ChIP-Seq on mouse liver cells, a full accounting of all RXRα binding sites and of RXRa related gene regulations is expected to address the main knowledge gap around RXRα. Liver tissue of wild type and hs-RXRa-del-exon4-/- mice, male and female for each genotype have been ChIP-Seq'ed for RXRa and Pol2.
2014-04-01 | E-GEOD-21696 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE18390: Effects of retinoids on estrogen-receptor-positive and -negative breast carcinoma cells: mRNA profiling GSE18628: MicroRNA profiling shows different response to retinoids in estrogen-receptor positive and negative cells Refer to individual Series
2010-05-21 | E-GEOD-18693 | biostudies-arrayexpress
Project description:Comparison between ChIP-Seq data of RAR? and RAR?, between RAR and RXR, as well as between control and retinoic acid-treatment for each investigated nuclear receptors. Mouse were treated by control diet and RA-diet for 1 days. After treatment, livers were used to do ChIP using antibodies of RXR?, RAR?, and RAR?. An aliquote of total chromatin without pull-down process by any antibodies was used as input control. A single-end read of 35bp sequencing was performed on each of ChIPed DNA and input. Sequencing data of RAR? and RAR? were compared to each other. In addtional, each of RAR? and RAR? data were compared with RXR? data. For each nuclear receptor, ChIP-Seq data prior or after RA-treatment were also compared with each other.
2014-01-23 | E-GEOD-53736 | biostudies-arrayexpress
Project description:Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors comprising retinoic acid (RARa,b,g) and retinoid X (RXRa,b,g) receptors. How a single signal induces highly complex temporally controlled networks that ultimately orchestrate physiological processes is unclear. Using an RA-inducible differentiation model we defined the temporal changes in the genome-wide binding patterns of RARg and RXRa and correlated them with transcription regulation. Unexpectedly, both receptors displayed a highly dynamic binding, with different RXRa heterodimers targeting identical loci. Comparison of RARg and RXRa co-binding at RA-regulated genes identified putative RXRa-RARg target genes that were validated with subtype-selective agonists. Gene regulatory decisions during differentiation were inferred from transcription factor target gene information and temporal gene expression. This analysis revealed 6 distinct co-expression paths of which RXRa-RARg is associated with transcription activation, while Sox2 and Egr1 were predicted to regulate repression. Finally, RXRa-RARg regulatory networks were reconstructed through integration of functional co-citations. Our analysis provides a dynamic view of RA signalling during cell differentiation, reveals RA heterodimer dynamics and promiscuity, and predicts decisions that diversify the RA signal into distinct gene-regulatory programs. RXRa; RARg and RNA Polymerase II chromatin binding has been assessed at five time points; in addition an input control for F9 cells as well as a RXRa ChIP-seq assay from a rxra-/- ko strain has been performed.
2011-10-11 | E-GEOD-30538 | biostudies-arrayexpress
Project description:Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in heart failure. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during the evolution of heart failure. BET inhibition suppresses cardiomyocyte hypertrophy in a cell-autonomous manner, confirmed by RNA interference in vitro. Following both pressure overload and neurohormonal stimulation, BET inhibition potently attenuates pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to activation of canonical master regulators and effectors that are central to heart failure pathogenesis. Specifically, BET bromodomain inhibition in mice abrogates pathology-associated pause release and transcriptional elongation, thereby preventing activation of cardiac transcriptional pathways relevant to the gene expression profile of failing human hearts. This study implicates epigenetic readers in cardiac biology and identifies BET co-activator proteins as therapeutic targets in heart failure. ChIP-Seq of mouse heart tissues from mice induced with heart failure and treated with JQ1 BET bromodomain inhibitor
2013-08-06 | E-GEOD-46668 | biostudies-arrayexpress
Project description:Children with Down syndrome (DS) have a 20-fold increased risk of developing B cell acute lymphoblastic leukemia (B-ALL). Polysomy 21 (i.e., extra copies of chr.21) is also the most frequent somatic aneuploidy among all B-ALLs. Additional B-ALLs harbor intrachromosomal amplifications of chr.21q22 (iAMP21). Yet, the mechanistic links between chr.21q22 triplication and B-ALL remain undefined. Here we show that germline triplication of only 31 genes orthologous to human chr.21q22 is sufficient to confer murine B cell self-renewal in vitro, B cell maturation defects in vivo, and B-ALL in concert with either BCR-ABL or CRLF2 with activated JAK2. Chr.21q22 triplication suppresses H3K27me3 in murine progenitor B cells and B-ALLs, and ÒbivalentÓ genes with both H3K27me3 and H3K4me3 at their promoters in wild-type progenitor B cells are preferentially overexpressed in triplicated cells. Strikingly, human B-ALLs with polysomy 21 are distinguished by their overexpression of genes known to be marked with H3K27me3 in multiple cell types. Finally, overexpression of HMGN1, a nucleosome remodeling protein encoded on chr.21q22, suppresses H3K27me3 and promotes both B cell proliferation in vitro and B-ALL in vivo. These data implicate HMGN1 overexpression and loss of H3K27me3 in progenitor B cell transformation and suggest strategies to target leukemias with polysomy 21. ChIP-seq in wild-type and Ts1Rhr B cell progenitors for H3K27ac and H3K4me3
2014-04-20 | E-GEOD-48534 | biostudies-arrayexpress
Project description:The overall study explores differential sensitivity of estrogen-receptor-positive and -negative breast carcinoma cells to retinoids via gene expression and microRNA profiling in MCF7 and MDA-MB-231 cells. This Series reports results of transcriptional profiling of breast carcinoma cell lines comparing the effects of retinoic acid treatment (6 and 48 hours) on estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells.
2010-05-21 | GSE18390 | GEO
Project description:The aim of the experiment was to gain insight into the role of estrogen receptor beta (ERβ) isoforms in the response of breast cancer MCF7 cells to antiestrogens and retinoids. To this end, clones of MCF7 cells constitutively expressing human ERβ1 (MCF7-ERβ1) or ERβ2 (MCF7-ERβ2) were established and used for the determination of the global transcriptional changes induced upon treatment with hydroxytamoxifen (OHT) and all-trans retinoic acid (ATRA). Gene signatures associated with each clone will shed light to the mechanism underlying the ERβ1- and ERβ2-mediated response of MCF7 cells to antiestrogens and retinoids.
2022-12-13 | E-MTAB-12549 | biostudies-arrayexpress
Project description:Alterations of IKZF1, encoding the lymphoid transcription factor IKAROS, are a hallmark of high risk acute lymphoblastic leukemia (ALL), however the role of IKZF1 alterations in ALL pathogenesis is poorly understood. Here we show that in mouse models of BCR-ABL1 leukemia, Ikzf1 and Arf alterations synergistically promote the development of an aggressive lymphoid leukemia. Ikzf1 alterations were associated with acquisition of stem cell-like features, including self-renewal and increased bone marrow stromal adhesion. Rexinoid receptor agonists reversed this phenotype, in part by inducing expression of IKZF1, resulting in abrogation of adhesion and self-renewal, cell cycle arrest and attenuation of proliferation without direct cytotoxicity. Retinoids potentiated the activity of dasatinib in mouse and human BCR-ABL1 ALL, providing a new therapeutic option in IKZF1-mutated ALL. Significance: The outcome of therapy for high-risk acute lymphoblastic leukemia remains suboptimal despite contemporary chemotherapy and the advent of targeted therapeutic approaches. Recent genomic studies have identified deletions or mutations of IKZF1 as a hallmark of high-risk ALL, but an understanding of how IKZF1 alteration contribute to leukemia development are lacking. Here we show that IKZF1 alterations drive lymphoid lineage, a stem cell-like phenotype, abnormal bone marrow adhesion, and poor responsiveness to tyrosine kinase inhibitor (TKI) therapy. Using a high-content screen, we show that retinoids reverse this phenotype in part by inducing expression of wild type IKZF1, and increase responsiveness to TKIs. These findings provide new insight into the pathogenesis of high-risk ALL and potential new therapeutic approaches.
2015-09-04 | GSE68391 | GEO