Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

ABSTRACT: Febrile temperature enhanced Th17 differentiation in Smad4 SUMOylation-dependent manner. Smad4-deficiency impaired the febrile temperature-enhanced Th17 differentiation. In order to understand how febrile temperature and Smad4 contribute to Th17 pathogenicity, we conducted transcriptional analysis of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C (Day 3).

ORGANISM(S): Mus musculus

PROVIDER: GSE125264 | GEO | 2020/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

Project description:Smad4 was required for febrile temperature enhanced Th17 differentiation. In order to further understand the mechanisms whereby Smad4 enhance Th17 differentiation, we conducted ChIP-seq analysis of Smad4 in Th17 cells cutured 37°C and 39.5°C after 24 hours.

2020-06-26 | GSE125263 | GEO

ChIP-Seq of Smad4 in Th17 cells cultured at 37°C and 39.5°C and RNA-Seq of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

Project description:ChIP-Seq of Smad4 in Th17 cells cultured at 37°C and 39.5°C and RNA-Seq of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

| PRJNA515712 | ENA

Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation

Project description:Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

2017-10-25 | GSE101527 | GEO

Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation [ChIP-seq]

Project description:Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

2017-10-25 | GSE101593 | GEO

Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

Project description:Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C

| PRJNA515709 | ENA

Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

Project description:Genome binding/occupancy profiling of Smad4 in Th17 cells cultured at 37°C and 39.5°C after 24 hours.

| PRJNA515714 | ENA

mouse CD4+ T cells IP-MS - Reversing SKI-SMAD4-mediated suppression is essential for TH17 cell differentiation

Project description:Identifying Smad4-binding proteins in mouse CD4+ T cells under IL6SB condition. Mouse CD4+ T cells were isolated from mouse spleen and lymph nodes.

2017-10-26 | PXD007172 | Pride

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

Tripartite motif-containing 33 (Trim33) determines the pathogenic function of Th17 cells

Project description:We report that Tripartite motif-containing 33 (Trim33), a protein that was previously associated with TGF-beta signaling, determines the pathogenic function of Th17 cells. Trim33 deficiency in T cells resulted in resistance to an autoimmune disease model. Lack of Trim33 did not impact TGF-beta signaling in mediating Foxp3 gene expression but greatly reduced TGF-beta induction of IL-17 production during Th17 cell differentiation. Importantly, we found TGF-beta not only increased IL-17 but also suppressed IL-10 expression; absence of Trim33 or Smad2 but not Smad4 in T cells enhanced IL-10 expression. In a Smad2-dependent manner, Trim33 was recruited to Il17 and Il10 gene loci and was crucial in appropriate histone modification accompanying Th17 differentiation. Our study thus demonstrates that Trim33, a non-canonical branch of TGF-beta signaling, programs the pro-inflammatory function of Th17 differentiation by promoting IL-17 and suppressing IL-10 expression. As a critical switch of pathogenic versus regulatory phenotype of T cells, Trim33 may be targeted in treating human autoimmune diseases.

2018-05-02 | GSE113925 | GEO

Human Th17 Cell differentiation

Project description:The early stages of human Th17 Cell differentiation were studied using label free proteomics to compare Th17 polarized CD4+ human T cells at 24 h and 72 h with activated cells (72 and 24 h) and Thp cells.

2019-01-28 | PXD008973 | Pride

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