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Essential functions of the Glucocorticoid Receptor require direct DNA binding [ChIP-seq]

ABSTRACT: Essential functions of the Glucocorticoid Receptor require direct DNA binding [ChIP-seq]

PROVIDER: PRJNA522805 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11731896_1.fastq.gz	Fastqsanger.gz
	SRR11731896_2.fastq.gz	Fastqsanger.gz
	SRR11731897_1.fastq.gz	Fastqsanger.gz
	SRR11731897_2.fastq.gz	Fastqsanger.gz
	SRR11731898_1.fastq.gz	Fastqsanger.gz

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Essential functions of the Glucocorticoid Receptor require direct DNA binding

Project description:Essential functions of the Glucocorticoid Receptor require direct DNA binding

| PRJNA522804 | ENA

Essential functions of the Glucocorticoid Receptor require direct DNA binding [RNA-seq]

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Essential functions of the Glucocorticoid Receptor require direct DNA binding [ChIP-seq]

Project description:We performed ChIP-Sequencing for GR in GR wild-type, GR Zn mutant and GR Knock-Out Mouse Embryonic Fibroblasts (MEFs). We show that GR Zn mutant chromatin binding is mostly lost except for some tethered binding sites. Together with the corresponding RNA-Seq data, our results illustrate how GR requires direct DNA binding for activation and repression of target genes.

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Essential functions of the Glucocorticoid Receptor require direct DNA binding

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

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Essential functions of the Glucocorticoid Receptor require direct DNA binding [RNA-seq]

Project description:We performed RNA sequencing in Mouse Embryonic Fibroblasts (MEFs) of GR wild-type and GR Zn. Cells were treated with: vehicle (EtOH), Dexamethasone (Dex), Lipopolysaccharide (LPS) or Dex+LPS. We show that GR Zn does not regulate any GR target gene

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Anti-inflammatory functions of the glucocorticoid receptor require DNA binding.

Project description:The glucocorticoid receptor is an important immunosuppressive drug target and metabolic regulator that acts as a ligand-gated transcription factor. Generally, GR's anti-inflammatory effects are attributed to the silencing of inflammatory genes, while its adverse effects are ascribed to the upregulation of metabolic targets. GR binding directly to DNA is proposed to activate, whereas GR tethering to pro-inflammatory transcription factors is thought to repress transcription. Using mice with a point mutation in GR's zinc finger, that still tether via protein-protein interactions while being unable to recognize DNA, we demonstrate that DNA binding is essential for both transcriptional activation and repression. Performing ChIP-Seq, RNA-Seq and proteomics under inflammatory conditions, we show that DNA recognition is required for the assembly of a functional co-regulator complex to mediate glucocorticoid responses. Our findings may contribute to the development of safer immunomodulators with fewer side effects.

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