Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15844622_1.fastq.gz	Fastqsanger.gz
	SRR15844622_2.fastq.gz	Fastqsanger.gz
	SRR15844623_1.fastq.gz	Fastqsanger.gz
	SRR15844623_2.fastq.gz	Fastqsanger.gz
	SRR15844624_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

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

Long Intergenic Noncoding RNA MIAT Contributes to Human Th17 Cell Differentiation

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. RNA-seq analysis identified genes implicated in Th17 differentiation and functions as MIAT targets. Our data suggests that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation.

2022-05-25 | GSE183664 | GEO

Chromatin Accessibility Analysis of LIRIL2R-Deficient and LIRIL2R-Sufficient Induced Regulatory T Cells

Project description:Chromatin Accessibility Analysis of LIRIL2R-Deficient and LIRIL2R-Sufficient Induced Regulatory T Cells

| PRJNA915967 | ENA

Long Intergenic Noncoding RNA MIAT Contributes to Human Th17 Cell Differentiation

Project description:Long Intergenic Noncoding RNA MIAT Contributes to Human Th17 Cell Differentiation

| PRJNA761653 | ENA

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

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

Trancriptional comparison of Zbtb32-deficient and -sufficient cells

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

| PRJNA325278 | ENA

Transcriptome profiling of left ventricles from systemic MIAT knockout mice

Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from systemic MIAT knockout (KO) mice were performed to identify novel MIAT targets in the heart.

2022-01-10 | GSE185396 | GEO

Gene expression analysis of WT Th17 versus STAT4 deficient Th17 cells from EAE mice

Project description:The purpose of this study is to compare transcriptional profiles of WT and STAT4-deficient Th17 cultured cells from mice with experimental autoimmune encephalomyelitis (EAE) using RNA sequencing. WT and STAT4 deficient splenocytes from EAE immunized mice were cultured with MOG peptide under Th17 conditions for three days, and then total RNA was extracted from CD4 T cells for sequencing. Differential gene expression was determined using the DESeq2 algorithm. These data reveal a previously unrecognized role for STAT4 in Th17 gene expression and function.

2023-03-30 | GSE227049 | GEO

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