Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation

ABSTRACT: STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation

PROVIDER: PRJNA510664 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation [array]

Project description:STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation [array]

| PRJNA510667 | ENA

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation [RNA-Seq]

Project description:STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation [RNA-Seq]

| PRJNA510663 | ENA

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation [array]

Project description:T helper 17 (Th17) cell differentiation triggered by interleukin-6 (IL-6) via STAT3 activation promotes inflammation in inflammatory bowel disease (IBD) patients. However, leukemia inhibitory factor (LIF), an IL-6 family cytokine, restricts inflammation by blocking Th17 cell differentiation via an unknown mechanism. Here, we report that microbiota dysregulation promotes LIF secretion by intestinal epithelial cells (IECs) in a mouse colitis model. LIF greatly activates STAT4 phosphorylation on multiple SPXX elements within the C-terminal transcription regulation domain. STAT4 and STAT3 act reciprocally on both canonical cis-inducible elements (SIEs) and noncanonical “AGG” elements at different loci. In lamina propria lymphocytes (LPLs), STAT4 activation by LIF blocks STAT3-dependent Il-17a/Il-17f promoter activation, whereas in IECs, LIF bypasses the extraordinarily low level of STAT4 to induce YAP gene expression via STAT3 activation. In addition, we found that the administration of LIF is sufficient to restore microbiome homeostasis. Thus, LIF effectively inhibits Th17 accumulation and promotes repair of damaged intestinal epithelium in inflamed colon, and serves as a potential therapy for IBD.

2019-12-18 | GSE124078 | GEO

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation [RNA-Seq]

Project description:We report that microbiota dysregulation promotes LIF secretion by intestinal epithelial cells (IECs) in a mouse colitis model. LIF greatly activates STAT4 phosphorylation on multiple SPXX elements within the C-terminal transcription regulation domain. STAT4 and STAT3 act reciprocally on both canonical cis-inducible elements (SIEs) and noncanonical “AGG” elements at different loci. In lamina propria lymphocytes (LPLs), STAT4 activation by LIF blocks STAT3-dependent Il-17a/Il-17f promoter activation, whereas in IECs, LIF bypasses the extraordinarily low level of STAT4 to induce YAP gene expression via STAT3 activation. In addition, we found that the administration of LIF is sufficient to restore microbiome homeostasis. Thus, LIF effectively inhibits Th17 accumulation and promotes repair of damaged intestinal epithelium in inflamed colon, and serves as a potential therapy for IBD.

2019-12-18 | GSE124077 | GEO

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation

Project description: Not available

| S-SCDT-EMBOJ-2018-99595 | biostudies-other

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation.

Project description: Not available

| S-EPMC6418461 | biostudies-literature

STAT4 activation by leukemia inhibitory factor confers a therapeutic effect on intestinal inflammation

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

2019-12-18 | GSE124079 | GEO

Divergent roles for STAT4 in shaping effector differentiation of ILC1 and NK cells during gut inflammation II

Project description:Natural killer (NK) cells and type 1 innate lymphoid cells (ILC1) require the transcription factor STAT4 to elicit rapid effector responses and protect against pathogens. Herein, by combining genetic and transcriptomic approaches, we revealed that STAT4 played an unexpected divergent role in regulating effector differentiation of murine ILC1 and NK cells, during intestinal inflammation. Stat4 deletion in Ncr1-expressing cells led to an increased generation of cytotoxic ILC1 in the inflamed large intestine. By contrast, Stat4-deficient NK cells showed impaired terminal differentiation, characterized by lower levels of IRF-8 and KLRG1. STAT4 expression in NCR+ innate lymphocytes restrained gut inflammation and controlled both systemic IFN-g levels and the number of type 2 adaptive T cells in the large intestine. Collectively our data shed light on shared and distinctive mechanisms of transcriptional regulation driven by STAT4 in NK cells and ILC1 required for protection during intestinal inflammation.

2023-09-28 | GSE210977 | GEO

Divergent roles for STAT4 in shaping effector differentiation of ILC1 and NK cells during gut inflammation I

2023-09-28 | GSE210483 | GEO

Assessing chromatin accessibility in WT and STAT4-/- ILC1s

Project description:STAT4 dynamically interacts with the genomic landscape and functions in modulating chromatin accessibility to influence gene expression. We aimed to evaluate the impact of STAT4 on chromatin accessibility of colonic lamina propria ILC1s. To address this aim, we sorted ILC1s from the colonic LP of unmanipulated C57BL/6 and STAT4-/- mice and performed the assay for transposase-accessible chromatin using sequencing (ATAC-seq).

2019-06-17 | GSE132769 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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