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Chromatin accessibility analysis of MIAT sufficient and MIAT deficient Th17 cells by ATAC-seq

ABSTRACT: Chromatin accessibility analysis of MIAT sufficient and MIAT deficient Th17 cells by ATAC-seq

PROVIDER: PRJNA762336 | ENA |

REPOSITORIES: ENA

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Chromatin accessibility analysis of MIAT sufficient and MIAT deficient Th17 cells by ATAC-seq

Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. We found that MIAT deficiency leads to chromatin accessibility at several loci including IL17A promoter.

2022-05-25 | GSE183918 | GEO

ATAC-seq of wild type and Stat3-deficient or Rorgt-deficient Th17 cells

Project description:ATAC-seq of wild type and Stat3-deficient or Rorgt-deficient Th17 cells

| PRJNA642729 | ENA

ATAC-seq of wild type and Stat3-deficient or Rorgt-deficient Th17 cells

Project description:STAT3 has a more profound effect on chromatin accessibility regulation than RORgt during Th17 cell differentiation.

2020-07-30 | GSE153442 | GEO

ATAC-seq Analysis of Chromatin Accessibility in p53 Deficient Spermatogonial Stem Cells for High Frequency Transformation into Pluripotent State

Project description:Spermatogonial stem cells (SSCs) could transform into pluripotent state in long term culture without introduction of exogenous factors. And p53 deficiency rescued SSCs from extensive cell apoptosis during transformation induced by rewriting of methylation profiles in SSCs. Notably, p53 is believed as a key bottle-neck for reprogramming. Based on these studies, we compared the difference of chromatin accessibility between SSCs from wild type and p53 deficient SSCs mice using ATAC-seq, to explore the potential mechanism at chromosome level. And RNA-Seq was subsequently exerted to verify the predicted genes and related pathways in SSCs transformation. This result further reveals the role of p53 in regulating SSCs fates, which provide hints new insight for understanding the biological characteristics of germline stem cells, basic and clinic researchand molecular mechanisms of reprogramming and tumorigenesis.

2021-10-08 | E-MTAB-10012 | biostudies-arrayexpress

ATAC-seq analysis of C1qbp sufficient and deficient CD8+ T cells sorted from mice post infection with LCMV Armstrong

Project description:This study is aimed to explore whether C1qbp deficiency affects the epigenetic modification during the differentiation stage of CD8+ T cells. Transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 5 post-infection with LCMV Armstrong were collected and treated for ATAC-seq. ATAC-Seq analysis provided sufficient but not necessary evidence of epigenetic changes between WT and C1qbp KO CD8+ T cells. Our study have shown that, on day 5 post-infection with LCMV Armstrong, even WT and C1qbp KO CD8+ T cells have different mRNA expressing profiling, the ATAC-seq shows slight changes in chromatin accessibility of indicated genes.

2021-06-09 | GSE176369 | GEO

ATAC-seq of gata5GFP+/- cells in WT and Gata5/6 deficient zebrafish embryos during gastrulation

Project description:Gata5/6 are essential regulators in zebrafish heart development. To understand how Gata5/6 affects the chromatin accessibility and regulates cardiac gene expression, we FACS-isolated GFP+ and GFP- cells from Tg(gata5:GFP) transgenic embryos in both control and Gata5/6 deficient embryos (injected with Gata5/6 morpholinos) and conducted ATAC-seq. We performed the experiments at 8 hours post fertilization, intending to dissect the role of Gata5/6 in the earliest step in cardiac lineage specification. We did 2-3 biological replicates for each sample. ATAC-seq libraries were made using previously published protocol (Buenrostro et al., Nat. Methods, 2013. DOI: 10.1038/nmeth.2688) and sequenced on Illumina Hiseq2500.

2021-12-31 | E-MTAB-10427 | biostudies-arrayexpress

Mouse gene expression in wild-type Th17 cells and Pten deficient Th17 cells

Project description:Transcriptional profiling of mouse Th17 cells comparing WT Th17 cells with Pten-deficient Th17 cells. Naïve CD4 T cells from each mice were cultured Th17 polarizing condition for 3 days. Goal was to determine the effects of Pten on global gene expression.

2017-08-10 | GSE102414 | GEO

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

RORA proximal enhancer regulates its expression during early human Th17 cell differentiation [ATAC]

Project description:Distal regulatory elements, such as enhancers, play a pivotal role in dictating cell identity by controlling the transcriptional status of specific cells. The comprehensive understanding of the epigenetic landscape, encompassing enhancer establishment and chromatin accessibility, during the differentiation of human Th17 cells remains incomplete. Leveraging ATAC-seq based chromatin accessibility profile along with the profiling of key histone marks we identified potential enhancers crucial for fate specification of Th17 cells. We found that 24 single nucleotide polymorphisms (SNPs) associated with autoimmune diseases were located near Th17-enhancers. Interestingly, these SNPs overlapped the binding sites of transcription factor active in Th17 cells. Among the Th17 specific enhancers, we identified an enhancer in the intron of RAR-related orphan receptor alpha (RORA) that was earlier predicted to regulate RORA expression. Functional validation through luciferase reporter assays confirmed that this enhancer positively regulate the transcription. Moreover, employing CRISPR-Cas9-mediated deletion of a transcription factor binding site-rich region within the identified RORA enhancer, we demonstrated its role in regulating RORA transcription. These findings provide insights into the potential mechanism by which the RORA enhancer modulates Th17 differentiation and into the role of regulatory SNPs within noncoding regions in conferring resistance or susceptibility to Th17 cell-mediated autoimmune pathologies.

2024-05-23 | GSE243058 | GEO

Trancriptional comparison of Zbtb32-deficient and -sufficient cells

Project description:Trancriptional comparison of Zbtb32-deficient and -sufficient cells

| PRJNA325278 | ENA