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Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages [RNA-seq]

ABSTRACT: Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages [RNA-seq]

PROVIDER: PRJNA433244 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6678050_1.fastq.gz	Fastqsanger.gz
	SRR6678050_2.fastq.gz	Fastqsanger.gz
	SRR6678060_1.fastq.gz	Fastqsanger.gz
	SRR6678060_2.fastq.gz	Fastqsanger.gz
	SRR6678051_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages

Project description:Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages

| PRJNA433364 | ENA

Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages [RNA-seq]

Project description:The Glucocorticoid Receptor (GR) potently represses macrophage-elicited inflammation, however, the underlying mechanisms remain obscure. Our genome-wide analysis reveals that pro-inflammatory paused genes, activated via global negative elongation factor (NELF) dissociation and RNA Polymerase (Pol)2 release from early elongation arrest, and non-paused genes, induced by de novo Pol2 recruitment, are equally susceptible to acute glucocorticoid repression. Moreover, in both cases the dominant mechanism involves rapid GR tethering to p65 at NF-kB binding sites. Yet, specifically at paused genes, GR activation triggers widespread promoter accumulation of NELF, with myeloid cell-specific NELF deletion conferring glucocorticoid resistance. Conversely, at non-paused genes, GR attenuates the recruitment of p300 and histone acetylation, leading to a failure to assemble BRD4 and Mediator at promoters and enhancers, ultimately blocking Pol2 initiation. Thus, GR displays no preference for a specific pro-inflammatory gene class, however, it effects repression by targeting distinct temporal events and components of transcriptional machinery

2018-02-28 | GSE110243 | GEO

Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages [ChIP-seq]

2018-02-28 | GSE109131 | GEO

Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages [ChIP-seq]

Project description:Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages [ChIP-seq]

| PRJNA429743 | ENA

Gene-specific mechanisms dictate glucocorticoid receptor-mediated repression of inflammatory response genes in macrophages

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

2018-02-28 | GSE110279 | GEO

Gene-specific mechanisms direct glucocorticoid-receptor-driven repression of inflammatory response genes in macrophages.

Project description:The glucocorticoid receptor (GR) potently represses macrophage-elicited inflammation, however, the underlying mechanisms remain obscure. Our genome-wide analysis in mouse macrophages reveals that pro-inflammatory paused genes, activated via global negative elongation factor (NELF) dissociation and RNA Polymerase (Pol)2 release from early elongation arrest, and non-paused genes, induced by de novo Pol2 recruitment, are equally susceptible to acute glucocorticoid repression. Moreover, in both cases the dominant mechanism involves rapid GR tethering to p65 at NF-kB-binding sites. Yet, specifically at paused genes, GR activation triggers widespread promoter accumulation of NELF, with myeloid cell-specific NELF deletion conferring glucocorticoid resistance. Conversely, at non-paused genes, GR attenuates the recruitment of p300 and histone acetylation, leading to a failure to assemble BRD4 and Mediator at promoters and enhancers, ultimately blocking Pol2 initiation. Thus, GR displays no preference for a specific pro-inflammatory gene class; however, it effects repression by targeting distinct temporal events and components of transcriptional machinery.

| S-EPMC5821458 | biostudies-literature

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

Analysis of local glucocorticoid receptor occupancy at glucocorticoid-repressed inflammatory enhancers in Beas-2B airway epithelial cells

Project description:This study combined ChIP-seq using two different GR antibodies and stable GR knockdown in Beas-2B airway epithelial cells to determine whether glucocorticoid-mediated repression of inflammatory enhancers requires local GR occupancy

2019-08-27 | GSE125623 | GEO

Analysis of local glucocorticoid receptor occupancy at glucocorticoid-repressed inflammatory enhancers in Beas-2B airway epithelial cells II

2019-08-27 | GSE135127 | GEO

Cryptochromes mediate rhythmic repression of the glucocorticoid receptor

Project description:The circadian transcriptional repressors cryptochromes 1 (Cry1) and 2 (Cry2) interact with the C-terminus of the glucocorticoid receptor (GR) and are required for transrepression in response to the synthetic GR ligand dexamethasone (Dex) in mouse embryonic fibroblasts. Dex induction of many genes was increased in Cry-deficient fibroblasts suggesting that cryptochromes oppose transactivation in addition to contributing to transrepression. In mice, genetic loss of Cry1 and/or Cry2 resulted in glucose intolerance and constitutively high levels of circulating corticosterone, suggesting reduced glucocorticoid suppression of the hypothalamic-pituitary-adrenal axis coupled with increased sensitivity to the hyperglycemic effects of glucocorticoid-mediated transactivation in the liver. Cry1 and Cry2 association with a GRE in the Pck1 promoter was stimulated by Dex, and Dex-induced transcription of pck1 was strikingly increased in Cry-deficient livers. Finally, cry1-/-;cry2-/- mice subjected to 8 weeks of chronic Dex treatment exhibited incomplete suppression of circulating corticosterone and greater glucose intolerance compared with wildtype littermates subjected to the same chronic treatment, consistent with enhanced transcriptional response to the synthetic glucocorticoid ligand. Total RNA was obtained from WT and Cry1/2 KO MEFs treated with Dexamethasone (1uM) or control EtOH for 16 hours.

2011-12-22 | E-GEOD-24469 | biostudies-arrayexpress

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