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Glucocorticoid receptor (GR) binding in primary macrophages isolated from WT and GRdim mice

ABSTRACT: We report ChIP-seq data for GR in bone marrow-derived primary macrophages isolated from WT and GRdim mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE59764 | GEO | 2015/04/14

SECONDARY ACCESSION(S): PRJNA256173

REPOSITORIES: GEO

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Glucocorticoid receptor (GR) binding in primary macrophages isolated from WT and GRdim mice

Project description:We report ChIP-seq data for GR in bone marrow-derived primary macrophages isolated from WT and GRdim mice. Examination of GR binding in WT and GRdim mice on a genome-wide scale

2015-04-14 | E-GEOD-59764 | biostudies-arrayexpress

Transcription factor binding in liver tissue isolated from WT and GRdim mice

Project description:We report ChIP-seq and ChIP-exo data for GR in liver tissue isolated from WT and GRdim mice. Comparison of the mouse models reveals that GR interacts with the genome as both a monomer and dimer. Examination of GR, RNAPII and CEBPb binding in WT and GRdim mice on a genome-wide scale

2015-04-14 | E-GEOD-59752 | biostudies-arrayexpress

Transcription factor binding in liver tissue isolated from WT and GRdim mice

2015-04-14 | GSE59752 | GEO

Genomic Redistribution of GR Monomers and Dimers Mediates the Transcriptional Response to Exogenous Glucocorticoid In Vivo.

Project description:Expression profiles of GRdim mutant macrophages (mouse, bone-marrow derived) treated with LPS for 6 hrs or with LPS (6hrs) + Dex (O/N 1uM). Identification of GR-regulated genes in response to LPS. 3 Grdim mutant macrophages samples treated with LPS (6hrs) and 3 Grdim mutant macrophage samples treated with LPS (6hrs) and Dex (overnight).

2015-04-23 | E-GEOD-68160 | biostudies-arrayexpress

Identification of glucocorticoid receptor (GR) binding sites in multiple myeloma

Project description:Purpose: The glucocorticoid receptor is widely expressed across mutliple tissues, and yet has very tissue specfic actions. This is most likely due to the tissue specific chormatin landscape which dictates GR binding. It identify GR tragets in myeloma as potential therapeutic targets, we have used ChIP-seq to identify myeloma specific GR binding sites. Methods: DNA-chromatin complexes were isolated from MM.1S (GR positive) or MM.1RL (GR negative) cells following a 2 hour treatment with either 1 micromolar dexamethasone or vehicle control. Complexes were immunoprecipitated with either a GR specific antibody or an IgG control and the DNA isolated for next generation sequencing. Results: We identified 8689 high confidence GR binding sites and further correlated those sites to specific genes which are regulated by glucocorticoids through integration with gene expression array data from our lab (submitted to GEO speparately). Conclusions: Overall, our results indentified nearly 400 genes under the direct transcriptional control of glucocorticoids in myeloma cells.

2015-12-22 | GSE63209 | GEO

Genomic Redistribution of GR Monomers and Dimers Mediates the Transcriptional Response to Exogenous Glucocorticoid In Vivo.

2015-04-23 | GSE68160 | GEO

Prednisolone-induced differential gene expression in liver of mice carrying the wild type or a dimerization-defective glucocorticoid receptor

Project description:Glucocorticoids control expression of a large number of genes after binding to the glucocorticoid receptor (GR). Transcription may be regulated either by binding of the GR dimer to DNA regulatory elements or by protein-protein interactions of GR monomers with other transcription factors. Although the type of regulation for a number of individual target genes is known, the relative contribution of both mechanisms to the regulation of the entire transcriptional program remains elusive. To study the importance of GR dimerization in regulation of gene expression, we performed gene expression profiling in liver of prednisolone-treated wild type (WT) and genetically engineered mice that have lost the ability to form GR-dimers (GRdim). Mice carrying a wild type (WT) glucocorticoid receptor or a dimerization-defective glucocorticoid receptor (GRdim) were treated subcutaneous with vehicle or prednisolone (1mg/kg) and sacrificed 150 minutes later. From the livers of these mice total RNA was extracted, processed and hybridized on Affymetrix microarrays. In total 24 mice (6 vehicle-treated WT mice, 6 prednisolone-treated WT mice, 6 vehicle-treated GRdim mice and 6 prednisolone-treated GRdim mice) were included in the study.

2010-06-08 | E-GEOD-21048 | biostudies-arrayexpress

Genome-wide Binding Potential and Regulatory Activity of the Glucocorticoid Receptor’s Monomeric and Dimeric Forms

Project description:A widely regarded model for glucocorticoid receptor (GR) action postulates that dimeric binding to DNA regulates unfavorable metabolic pathways while monomeric receptor binding promotes repressive gene responses related to its anti-inflammatory effects. This model has been built upon the characterization of the GRdim mutant, reported to be incapable of DNA binding and dimerization. Although quantitative live-cell imaging data shows GRdim as mostly dimeric, genomic studies, on the basis of recovery of enriched half-site response elements, suggest monomeric engagement on DNA. Here, we performed genome-wide studies on GRdim and a constitutively monomeric mutant. Our results show that impairing dimerization affects binding to even open chromatin. Also, GRdim does not exclusively bind half-response elements. Our results do not support a physiological role for monomeric GR and are consistent with a common mode of receptor binding via higher order structures that drives both the activating and repressive actions of glucocorticoids.

2021-01-19 | GSE117661 | GEO

Glucocorticoid receptor dimers control intestinal STAT1-mediated IFN- and TNF-induced inflammation in mice

Project description:Tumor Necrosis Factor (TNF) is an important mediator in numerous inflammatory diseases, e.g. in inflammatory bowel diseases (IBD). In IBD, acute increases in TNF production can lead to disease flares. Glucocorticoids (GCs), which are steroids that bind and activate the glucocorticoid receptor (GR), are able to protect animals and humans against acute TNF-induced inflammatory symptoms. Mice with a poor transcriptional response of GR-dimer-dependent target genes were studied in a model of TNF-induced lethal inflammation. In contrast to the GRwt/wt mice, these GRdim/dim mice displayed a significant increase in TNF sensitivity and a lack of protection by the GC dexamethasone (DEX). Unchallenged GRdim/dim mice had a strong interferon-stimulated gene (ISG) signature, along with STAT1 upregulation and phosphorylation. This ISG signature was gut specific and, based on our studies with antibiotics, depended on the gut microbiota. GR dimers directly bound to short DNA sequences in the STAT1 promoter known as inverted repeat negative GRE (IR-nGRE) elements. Poor control of STAT1 in GRdim/dim mice led to failure to repress ISG genes resulting in excessive necroptosis induction by TNF. Our findings support a critical interplay between gut microbiota, interferons, necroptosis and GR in both the basal response to acute inflammatory challenges and in the pharmacological intervention by GCs.

2018-04-26 | GSE113691 | GEO

ChIP-MS of Glucocorticoid Receptor in primary mouse macrophages

Project description:Glucocorticoids (GCs) are the most effective anti-inflammatory drugs in current clinical settings, yet their genomic modes of action are poorly understood. GCs bind to the Glucocorticoid Receptor (GR), which acts as a transcription factor to control gene expression in the immune system. Understanding the molecular mechanism that delineates gene repression of pro-inflammatory target genes from gene activation of metabolic genes will help to improve GC therapy and overcome adverse effects.

2021-09-09 | PXD018077 | Pride

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