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Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [ATAC-Seq]

ABSTRACT: Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [ATAC-Seq]

PROVIDER: PRJNA600864 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10876051_1.fastq.gz	Fastqsanger.gz
	SRR10876051_2.fastq.gz	Fastqsanger.gz
	SRR10876052_1.fastq.gz	Fastqsanger.gz
	SRR10876052_2.fastq.gz	Fastqsanger.gz
	SRR10876053_1.fastq.gz	Fastqsanger.gz

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Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3

Project description:Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3

| PRJNA600856 | ENA

Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [RNA-Seq]

Project description:We analysed the transcriptomic gene signature of day 3 CD8+ T cell effectors in the absence of NR4A3 to determine the impact of this transcription factor on early transcriptomic programming of CD8 T cell memory and function

2020-08-24 | GSE143512 | GEO

Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [RNA-Seq]

Project description:Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [RNA-Seq]

| PRJNA600865 | ENA

Early programming of CD8+ T cell response by the orphan nuclear receptor NR4A3 [ATAC-Seq]

Project description:We analysed the chromatin opening and accessibillity of transcription factor binding motifs of in vitro activated OT-I CD8+ T cells in the absence of NR4A3 to determine the early impact of NR4A3 in CD8 T cell differentiation

2020-08-24 | GSE143511 | GEO

The orphan nuclear receptor NR4A3 is involved in the function of dendritic cells

Project description:Transcriptome analysis of LPS-stimulated bone marrow-derived dendritic cells with NR4A3 gene silencing The NR4A3/NOR1 belongs to the NR4A subfamily of the orphan nuclear hormone receptor superfamily, which is activated in a ligand-independent manner. To examine the role of NR4A3/NOR1 in gene expression of dendritic cells (DCs), we introduced NR4A3 siRNA into bone marrow-derived DCs (BMDCs) and determined the expression levels of mRNA and proteins of cytokines, cell surface molecules, NFκB signaling-related proteins, and transcription factors. The expression level of NR4A3 was markedly up-regulated by TLRs-mediated stimulation in DCs. NR4A3 knockdown significantly suppressed LPS, CpG, or poly I:C-mediated up-regulation of CD80, CD86, IL-10, IL-6, and IL-12. Proliferation and IL-2 production levels of T cells co-cultured with NR4A3-knocked down DCs were significantly lower than that of T cells co-cultured with control DCs. Furthermore, the expression of IKKβ, IRF4, and IRF8 was significantly decreased in NR4A3 siRNA-introduced BMDCs. The knockdown experiments using siRNAs for IKKβ, IRF4, and/or IRF8 indicated that LPS-induced up-regulation of IL-10 and IL-6 was reduced in IKKβ knocked down cells, and that the up-regulation of IL-12 was suppressed by the knockdown of IRF4 and IRF8. Taken together, these results indicate that NR4A3 is involved in TLR-mediated activation and gene expression of DCs.

2017-10-01 | GSE101831 | GEO

Early programming of CD8<sup>+</sup> T cell response by the orphan nuclear receptor NR4A3.

Project description:Enhancing long-term persistence while simultaneously potentiating the effector response of CD8+ T cells has been a long-standing goal in immunology to produce better vaccines and adoptive cell therapy products. NR4A3 is a transcription factor of the orphan nuclear receptor family. While it is rapidly and transiently expressed following T cell activation, its role in the early stages of T cell response is unknown. We show that NR4A3-deficient murine CD8+ T cells differentiate preferentially into memory precursor and central memory cells, but also produce more cytokines. This is explained by an early influence of NR4A3 deficiency on the memory transcriptional program and on accessibility of chromatin regions with motifs for bZIP transcription factors, which impacts the transcription of Fos/Jun target genes. Our results reveal a unique and early role for NR4A3 in programming CD8+ T cell differentiation and function. Manipulating NR4A3 activity may represent a promising strategy to improve vaccination and T cell therapy.

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NR4A3 plays a pivotal role in the differentiation of monocyte-derived dendritic cells

Project description:The molecular requirements that guide the differentiation of monocytes into macrophages or monocyte-derived dendritic cells (Mo-DCs) are poorly understood. Here, we demonstrate that the nuclear orphan receptor NR4A3 guides monocyte fate and is essential for Mo-DC differentiation. Nr4a3-/- mice are impaired in the in vivo generation of DC-SIGN+ Mo-DCs following LPS stimulation and, as such, are defective at priming a CD8+ T cell response to gram negative bacteria. We also demonstrate that NR4A3 is an essential downstream effector of IRF4 during in vitro differentiation of Mo-DCs with GM-CSF and IL-4 and that, in absence of NR4A3, monocytes are diverted to macrophages. Our transcriptomic analysis of the genes regulated by NR4A3 reveals that the acquisition of the Mo-DC differentiation program is intertwined with the acquisition of a migratory signature. Furthermore, NR4A3 is critical for steady-state migration of non-lymphoid tissue conventional DCs to lymph nodes. Altogether, our results highlight a unique role for NR4A3 in Mo-DC differentiation and in the acquisition of migratory properties.

2019-06-25 | GSE99837 | GEO

Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

Project description:Medial arterial calcification is a chronic systemic vascular disorder distinct from atherosclerosis and is commonly observed in patients with chronic kidney disease (CKD), diabetes mellitus, and aging individuals. We previously showed that orphan nuclear receptor NR4A3 is a key regulator in the progression of apolipoprotein (apo) A-IV-induced atherosclerosis; however, little is known about its role in vascular calcification. NR4A3 expression was upregulated in calcified aortic tissues from CKD mice or 1,25(OH)2VitD3 overload-induced mice, and in human calcified aorta. NR4A3 deficiency preserved VSMCs contractile phenotype, inhibited the expression of osteoblast differentiation-related genes, and reduced calcium deposition in the vasculature.

2024-05-14 | GSE254075 | GEO

Effect of depletion of NR4A3 on vascular calcification [RNA-seq]

2024-05-14 | GSE254077 | GEO

Effect of depletion of NR4A3 on vascular calcification [CUT&Tag_NR4A3]

2024-05-14 | GSE254076 | GEO