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ABSTRACT: Global studies of Nur77 on metabolism of zebrafish

PROVIDER: PRJNA801348 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17793192.fastq.gz	Fastqsanger.gz
	SRR17793193.fastq.gz	Fastqsanger.gz
	SRR17793194.fastq.gz	Fastqsanger.gz
	SRR17793195.fastq.gz	Fastqsanger.gz
	SRR17793196.fastq.gz	Fastqsanger.gz

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Project description:Global studies of Nur77 on metabolism of zebrafish

| PRJNA801348 | ENA

Nuclear receptor Nur77 and Yin-Yang 1 synergistically increase mitochondrial abundance and activity in macrophages [ChIP-seq]

Project description:Mitochondrial biogenesis requires precise regulation of both mitochondrial-encoded and nuclear-encoded genes. Nuclear receptor Nur77 is known to regulate mitochondrial metabolism in macrophages and skeletal muscle cells. Here, we compared genome-wide Nur77 binding site and target gene expression in these two cell types, which revealed conserved roles for this nuclear receptor in the regulation of nuclear-encoded mitochondrial ribosomal proteins (MRP) and enrichment of motifs for the transcription factor Yin-Yang 1 (YY1). We show that Nur77 and YY1 interact, that YY1 increases Nur77 activity, and that their binding sites are co-enriched at MRP gene loci. Nur77 and YY1 co-expression synergistically increases mitochondrial abundance and activity in macrophages but not skeletal muscle. As such, we identify a macrophage-specific Nur77-YY1 interaction that enhances mitochondrial metabolism.

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Nuclear receptor Nur77 and Yin-Yang 1 synergistically increase mitochondrial abundance and activity in macrophages [RNA-seq]

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Project description:Global studies microbial diversity from zebrafish intestines

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Genome-wide binding profiles of nuclear FGFR1, RXR? and Nur77 in pluripotent mouse Embryonic Stem Cells and during Retinoic Acid-induced differentiation

Project description:We report the genome-wide binding patterns of nuclear FGFR1, RXR? and Nur77 in pluripotenet mESC and as mESC differentiate towared a neuronal lineage in response to high levels of Retinoic Acid treatment in vitro. We also report the genome-wide incorporation of histone varant H3.3 into chromatin specifically during Retinoic Acid-induced differentiation. This study presents nuclear FGFR1 as a global factor that controls genomic function by binding within the promoters of thousands of genes, both alone and in cooperation with RXR, Nur77 and histone H3.3, by targeting consensus DNA sequences of diverse transcription factor families. As such, it identifies a previously unknown, multifaceted form of control of major ontogenic pathways and gene networks targeted by the nuclear form of FGFR1. Examination of nuclear FGFR1, RXR?, and Nur77 binding sites in 2 celluar states. Examination of H3.3 incorporation in 1 cellular state.

2015-05-01 | E-GEOD-65695 | biostudies-arrayexpress

Nur77 overexpression in mouse skeletal muscle

2015-02-04 | GSE65585 | GEO

Nur77 overexpression in mouse skeletal muscle

Project description:We isolated total RNA from gastrocnemius muscle of wildtype and muscle-specific Nur77 overexpressing transgenic mice to identify Nur77-mediated changes in gene expression. Findings confirmed changes in genes involved in carbohydrate metabolism and muscle development. 2 replicate Illumina Single Color Mouse WG-6_V2_0 chips were used. 6 wildtype and 6 transgenic mice overexpressing Nur77 in skeletal muscle were used. RNA was isolated by Trizol and further purified through RNEasy column. RNA from 2 mice were pooled, for a total of 6 samples -- 3 wildtype and 3 transgenic. The same samples were split into two technical replicate chips. Each chip contains 3 wildtype and 3 transgenic samples.

2015-02-04 | E-GEOD-65585 | biostudies-arrayexpress

Nuclear receptor Nur77 limits the macrophage inflammatory response by reprogramming mitochondrial metabolism (ChIP-seq)

Project description:Activation of macrophages by inflammatory stimuli leads to reprogramming of mitochondrial metabolism to support the production of pro-inflammatory cytokines. Hallmarks of this metabolic rewiring are downregulation of α-ketoglutarate formation via isocitrate dehydrogenase (IDH) and accumulation of glutamine-derived succinate, which enhances the inflammatory response via the activity of succinate dehydrogenase (SDH). Here, we identify the nuclear receptor Nur77 (Nr4a1) as a key regulator of the pro-inflammatory metabolic switch in macrophages. Nur77-deficient macrophages fail to downregulate IDH expression and accumulate higher levels of succinate and other downstream TCA cycle metabolites in response to an inflammatory stimulus. Consequently, these macrophages produce more nitric oxide and pro-inflammatory cytokines in an SDH-dependent manner. In vivo, bone marrow Nur77 deficiency exacerbates atherosclerosis development and leads to increased systemic succinate levels. In conclusion, Nur77 supports an anti-inflammatory metabolic state in macrophages that protects against chronic inflammatory diseases such as atherosclerosis.

2018-08-21 | GSE102393 | GEO

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Project description:Knock out Nur77 - Gene regulation studies in different organs

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Nuclear receptor Nur77 limits the macrophage inflammatory response by reprogramming mitochondrial metabolism (RNA-seq)

2018-08-21 | GSE102359 | GEO