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RNA-Seq of murine CD4 positive T cells isolated from Nur77-deficient mice and their Nur77-competent counterparts

ABSTRACT: RNA-Seq of murine CD4 positive T cells isolated from Nur77-deficient mice and their Nur77-competent counterparts

PROVIDER: PRJNA473083 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7217380.fastq.gz	Fastqsanger.gz
	SRR7217390.fastq.gz	Fastqsanger.gz
	SRR7217400.fastq.gz	Fastqsanger.gz
	SRR7217381.fastq.gz	Fastqsanger.gz
	SRR7217391.fastq.gz	Fastqsanger.gz

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RNA-Seq of murine CD4 positive T cells isolated from Nur77-deficient mice and their Nur77-competent counterparts

Project description:Endogenous changes in the nuclear encoded genes were analysed using RNA-Seq in order to compare the genetic profile of murine CD4 positive T cells isolated from Nur77-deficient mice and their Nur77-competent counterparts.

2018-07-30 | GSE114912 | 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 regulates immunomechanics of macrophages

Project description:Macrophages exhibit remarkable plasticity in their morphology and mechanics, enabling them to adapt and execute essential inflammatory functions, such as navigating through inflamed tissue and pathogen engulfment. However, the precise regulatory mechanisms governing these dynamic changes in macrophage mechanics during inflammation remain poorly understood. Although the involvement of nuclear receptor Nur77 in macrophage inflammation has been extensively investigated, its potential correlation with cellular mechanics has not been investigated. In this study, we employ cytoskeletal imaging, single-cell acoustic force spectroscopy (AFS), migration and phagocytosis experiments, and RNA-sequencing analysis on bone marrow-derived macrophages (BMDMs) to compare wild-type (WT) and Nur77-deficient (Nur77-KO) cells. Our findings reveal that Nur77-KO BMDMs exhibit changes to their actin networks compared to WT BMDMs, which is associated with a stiffer and more rigid phenotype. Subsequent in-vitro experiments validated our observations, showcasing that Nur77 deficiency leads to enhanced migration, reduced adhesion, and increased phagocytic activity. The transcriptomics data confirmed altered mechanics-related pathways in Nur77-deficient macrophage that are accompanied by a robust pro-inflammatory phenotype. Utilizing previously obtained ChIP-data, we revealed that Nur77 directly targets differentially expressed genes associated with cellular mechanics. In conclusion, while Nur77 is recognized for its role in reducing inflammation of macrophages by inhibiting the expression of pro-inflammatory genes, our study identifies a novel regulatory mechanism where Nur77 governs macrophage inflammation through the modulation of expression of genes involved in cellular mechanics.

2024-08-02 | GSE253423 | GEO

Nur77 overexpression in mouse skeletal muscle

2015-02-04 | GSE65585 | GEO

Knock out Nur77 - Gene regulation studies in different organs

Project description:Nur77 is an orphan member of the nuclear receptor superfamily that is expressed in various types of cells and mediates diverse biological processes. The knock out Nur77 has a mutation in exon 2. Ligands of the nuclear receptor are unknown. Keywords: Dual colour hybridisation on cDNA microarrays, Nur77, Knock out

2007-04-01 | GSE7016 | GEO

Effect of Nur77 on gene expression in white adipose tissue of fasted mice.

Project description:The aim was to study the effects of Nur77 on the white adipose tissue transcriptome after fasting. For this purpose we performed gene expression profiling of white adipose tissue from Nur77-/- mice and wildtype (Nur77+/+) littermates submitted to prolonged fasting using microarray analysis on >27k elements cDNA microarrays.

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Nur77-deficiency in bone marrow-derived macrophages modulates inflammatory responses, extracellular matrix homeostasis, phagocytosis and tolerance

Project description:The nuclear orphan receptor Nur77 (NR4A1, TR3, or NGFI-B) has been shown to exhibit an anti-inflammatory function in macrophages. To further elucidate the role of Nur77 in macrophage physiology, we compared the transcriptome of bone marrow-derived macrophages (BMM) from wild-type (WT) and Nur77-knockout (KO) mice both before and after stimulation with IL4 or LPS. Comparison of gene expression in bone marrow-derived macrophages, isolated from 3 wild-type (control) and 3 Nur77-/- mice (case), left untreated or stimulated in triplicate for 8 hours with LPS or IL-4

2016-03-01 | E-GEOD-68167 | biostudies-arrayexpress

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

2024-05-07 | GSE263316 | GEO

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

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Nur77-deficiency in bone marrow-derived macrophages modulates inflammatory responses, extracellular matrix homeostasis, phagocytosis and tolerance

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