Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RORa enforces stability of the T-helper-17 cell effector program (ATAC-Seq)

ABSTRACT: RORa enforces stability of the T-helper-17 cell effector program (ATAC-Seq)

PROVIDER: PRJNA685778 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13260079_1.fastq.gz	Fastqsanger.gz
	SRR13260079_2.fastq.gz	Fastqsanger.gz
	SRR13260080_1.fastq.gz	Fastqsanger.gz
	SRR13260080_2.fastq.gz	Fastqsanger.gz
	SRR13260081_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

RORa enforces stability of the T-helper-17 cell effector program

Project description:RORa enforces stability of the T-helper-17 cell effector program

| PRJNA685773 | ENA

RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq)

Project description:RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq)

| PRJNA685777 | ENA

RORa enforces stability of the T-helper-17 cell effector program (RNA-Seq)

Project description:RORa enforces stability of the T-helper-17 cell effector program (RNA-Seq)

| PRJNA685776 | ENA

RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq (2))

Project description:RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq (2))

| PRJNA685779 | ENA

RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq)

Project description:Chronic inflammation is responsible for a number of debilitating human diseases including inflammatory bowel disease, multiple sclerosis, and rheumatoid arthritis. The Th17 subset of T lymphocytes is an important player in the development of these pathogenic conditions. The transcription factor, RORgt was initially coined the master regulator of the Th17 program, but targeting RORgt therapeutically is dangerous owing to an enhanced risk of thymoma upon its inhibition. Another ROR family member, RORa, has also been implicated in Th17 function.

2022-10-25 | GSE163339 | GEO

RORa enforces stability of the T-helper-17 cell effector program (RNA-Seq)

2022-10-25 | GSE163338 | GEO

RORa enforces stability of the T-helper-17 cell effector program (ATAC-Seq)

2022-10-25 | GSE163340 | GEO

RORa enforces stability of the T-helper-17 cell effector program (ChIP-Seq (2))

2022-10-25 | GSE163341 | GEO

RORa enforces stability of the T-helper-17 cell effector program

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

2022-10-25 | GSE163342 | GEO

Genetic and pharmacological inhibition of the nuclear receptor RORa regulates Th17 driven inflammatory disorders

Project description:Full development of IL-17 producing CD4+ T helper cells (TH17 cells) requires the transcriptional activity of both orphan nuclear receptors RORa and RORgt. Despite this evidence, RORa is considered functionally redundant to RORgt; thus, the function and therapeutic value of RORa in TH17 cells remains underexplored. Using mouse models of autoimmune and chronic inflammation, we show that expression of RORa is required for TH17 cell pathogenicity. T-cell specific deletion of RORa reduced the development of experimental autoimmune encephalomyelitis (EAE) and colitis. Reduced inflammation was associated with decreased TH17 cell development, lower expression of tissue-homing chemokine receptors and integrins, and increased frequencies of Foxp3+ T regulatory (Treg) cells. Importantly, inhibition of RORa with a selective small molecule antagonist largely phenocopied our genetic data, potently suppressing the in vivo development of both chronic/progressive and relapsing/remitting EAE but had no effect on overall thymic cellularity. Furthermore, use of the RORa antagonist effectively inhibited human TH17 cell differentiation and memory cytokine secretion. Together, these data suggest that RORa acts independently of RORgt in programming TH17 pathogenicity and identifies RORa as a safer and more selective therapeutic target for the treatment of TH17-mediated autoimmunity.

2020-10-29 | GSE160327 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data