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Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ChIP-seq]

ABSTRACT: Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ChIP-seq]

PROVIDER: PRJNA479884 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10224549.fastq.gz	Fastqsanger.gz
	SRR10224550.fastq.gz	Fastqsanger.gz
	SRR10224551.fastq.gz	Fastqsanger.gz
	SRR10224552.fastq.gz	Fastqsanger.gz
	SRR10224553.fastq.gz	Fastqsanger.gz

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Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation.

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation.

| PRJNA479881 | ENA

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ATAC-seq]

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ATAC-seq]

| PRJNA479883 | ENA

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [RNA-seq]

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [RNA-seq]

| PRJNA479885 | ENA

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ATAC-seq]

Project description:Activation of T cells is dependent on organized and timely opening and closing of chromatin. We perform ATAC-seq (subseries 1), ChIP-seq (subseries 2), and RNA-seq (subseries 3) at 5, 24, and 60 h of T cell activation with anti-CD3 and -CD28 antibodies in human primary naïve CD4 T cells. We report that chromatin opening at early time points is established by AP-1 transcription factor and associated with transcriptional enhancer identified as risk loci for multiple immune diseases in human naïve CD4 T cells.

2019-10-16 | GSE116696 | GEO

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ChIP-seq]

2019-10-16 | GSE116695 | GEO

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [RNA-seq]

2019-10-16 | GSE116697 | GEO

AP-1 activity induced by co-stimulation is required for chromatin opening during T cell activation.

Project description:Activation of T cells is dependent on the organized and timely opening and closing of chromatin. Herein, we identify AP-1 as the transcription factor that directs most of this remodeling. Chromatin accessibility profiling showed quick opening of closed chromatin in naive T cells within 5 h of activation. These newly opened regions were strongly enriched for the AP-1 motif, and indeed, ChIP-seq demonstrated AP-1 binding at >70% of them. Broad inhibition of AP-1 activity prevented chromatin opening at AP-1 sites and reduced the expression of nearby genes. Similarly, induction of anergy in the absence of co-stimulation during activation was associated with reduced induction of AP-1 and a failure of proper chromatin remodeling. The translational relevance of these findings was highlighted by the substantial overlap of AP-1-dependent elements with risk loci for multiple immune diseases, including multiple sclerosis, inflammatory bowel disease, and allergic disease. Our findings define AP-1 as the key link between T cell activation and chromatin remodeling.

| S-EPMC7037242 | biostudies-literature

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation.

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

2019-10-16 | GSE116698 | GEO

AP-2γ is Required for Maintenance of Multipotent Mammary Stem Cells

Project description:Mammary gland ductal morphogenesis depends on the differentiation of mammary stem cells (MaSCs) into basal and luminal lineages. The AP-2γ transcription factor, encoded by Tfap2c, has a central role in mammary gland development but its effect in mammary lineages and specifically MaSCs is largely unknown. Herein, we utilized an inducible, conditional knockout of Tfap2c to elucidate the role of AP-2γ in maintenance and differentiation of MaSCs. Loss of AP-2γ in the basal epithelium profoundly altered the transcriptomes and decreased the number of cells within several clusters of mammary epithelial cells, including adult MaSCs and luminal progenitors. AP-2γ regulated the expression of genes known to be required for mammary development including Cebpb, Nfkbia, and Rspo1. As a result, AP-2γ-deficient mice exhibited repressed mammary gland ductal outgrowth and inhibition of regenerative capacity. The findings demonstrate that AP-2γ can regulate development of mammary gland structures potentially regulating maintenance and differentiation of multipotent MaSCs.

2020-12-30 | GSE143159 | GEO

The activity of early-life gene regulatory elements is hijacked in aging through pervasive AP-1–linked chromatin opening

Project description:The activity of early-life gene regulatory elements is hijacked in aging through pervasive AP-1–linked chromatin opening

| PRJNA924763 | ENA