Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

ABSTRACT: IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

PROVIDER: PRJNA419153 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon

Project description:The physiological stresses that diminish tissue stem-cell characteristics remain largely unknown. We previously reported that type I interferon (IFN), which is essential for host antiviral responses, is a physiological stressor for hematopoietic stem cells (HSCs) and that interferon regulatory factor-2 (IRF2), which attenuates IFN signaling, maintains the stemness of HSCs. Here, we explore the role of IRF2 in maintaining colonic epithelial stem cells (CoSCs). In mice with a conditional Irf2 deletion in the intestinal epithelium (hereafter Irf2ΔIEC mice), both the number and the organoid-forming potential of CoSCs was markedly reduced. Consistent with this finding, the ability of Irf2ΔIEC mice to regenerate colon epithelium after injury by dextran sodium sulfate (DSS) was severely impaired, independently of microbial dysbiosis. Mechanistically, CoSCs differentiated prematurely into transit-amplifying (TA) cells in Irf2ΔIEC mice, which might explain their low CoSC counts. A similar phenotype was induced in wild-type mice by repeated injections of low doses of poly(I:C), which induces type I IFN. Collectively, we demonstrated that chronic IFN signaling physiologically stresses CoSCs. This study provides new insight into the molecular mechanisms that maintain functional CoSCs throughout life.

2020-09-18 | GSE107142 | GEO

IRF2 maintains the stemness of colonic stem cells by limiting physiological stress from interferon.

Project description:The physiological stresses that diminish tissue stem-cell characteristics remain largely unknown. We previously reported that type I interferon (IFN), which is essential for host antiviral responses, is a physiological stressor for hematopoietic stem cells (HSCs) and small intestinal stem cells (ISCs) and that interferon regulatory factor-2 (IRF2), which attenuates IFN signaling, maintains their stemness. Here, using a dextran sodium sulfate (DSS)-induced colitis model, we explore the role of IRF2 in maintaining colonic epithelial stem cells (CoSCs). In mice with a conditional Irf2 deletion in the intestinal epithelium (hereafter Irf2?IEC mice), both the number and the organoid-forming potential of CoSCs were markedly reduced. Consistent with this finding, the ability of Irf2?IEC mice to regenerate colon epithelium after inducing colitis was severely impaired, independently of microbial dysbiosis. Mechanistically, CoSCs differentiated prematurely into transit-amplifying (TA) cells in Irf2?IEC mice, which might explain their low CoSC counts. A similar phenotype was induced in wild-type mice by repeated injections of low doses of poly(I:C), which induces type I IFN. Collectively, we demonstrated that chronic IFN signaling physiologically stresses CoSCs. This study provides new insight into the development of colitis and molecular mechanisms that maintain functional CoSCs throughout life.

| S-EPMC7479133 | biostudies-literature

IRF2 regulates macrophages apoptosis through a STAT1/3 and Caspase-1-dependent mechanism

Project description:Using microarray gene expression profiling of liver RNA samples rerived from IRF2+/+ and IRF2-/- mice treated with saline or LPS, we identified >40 genes that were significantly down-regulated in IRF2 -/- mice, including STAT3 which has been reported to regulate apoptosis. Keywords: compound treatment design We compared gene expression in IRF2+/+ and IRF2-/- mice treated with Saline or LPS for 3 or 6 hours. Two repeats were done for the LPS treatments. The total number of arrays is 6.

2007-09-01 | E-GEOD-5907 | biostudies-arrayexpress

Genome-wide maps of IRF2 targets

Project description:Using ChIP-seq technology, we tried to find out the whole genome targets for IRF2 in mouse colorectal cancer (CRC) cells. More than 7000 genes were defined as the target of IRF2.

2019-04-25 | GSE110175 | GEO

Gene expression profiling of mouse macrophages following IRF2 knockdown

Project description:We applied next-generation sequencing to investigate the gene expression profiles in mouse bone-marrow derived macrophages with or without IRF2 knockdown. We identified a number of differentially regulated genes in cells with IRF2 knockdown.

2017-11-18 | GSE106895 | GEO

Microarray of IRF2 overexpress in iKAP primary cultured cells (#3346)

Project description:We used microarrays to study the global gene expression and identified differentially expressed genes in IRF2-overexpressing 3346 iKAP cells, aiming to identify genes and pathways that are regulated by IRF2.

2019-04-25 | GSE109579 | GEO

IRF2 ChIP seq in mouse intestinal stem cells (ISCs)

Project description:To examine whether IRF2, a negative regulator of IFN signaling, constitutively represses IFN signaling by binding IFN-inducible gene loci in ISCs, we performed a genome-wide chromatin immunoprecipitation/DNA sequencing (ChIP-Seq) analysis of IRF2 in Lgr5 ISCs. We identified 381 binding peaks in these cells, including well-known IFN-inducible genes. Motif analysis showed significant enrichment of consensus-binding motifs for IRF transcription factors within these peaks. Within IRF2-occupied genes in ISCs, we identified 204 of experimentally validated IFN-inducible genes from Interferome database, and 10.8% of them were overlapped with the genes upregulated by type I IFN stimulation in ISCs. These findings indicated for the first time that IRF2 constitutively bound and repressed the sterile IFN signaling at the level of ISCs.

2020-07-21 | GSE137260 | GEO

IRF2 regulates macrophages apoptosis through a STAT1/3 and Caspase-1-dependent mechanism

2007-09-01 | GSE5907 | GEO

FIBP maintains colorectal cancer cells stemness via demethylation of stemness genes

Project description:FIBP maintains colorectal cancer cells stemness via demethylation of stemness genes

| PRJNA412214 | ENA

FIBP maintains colorectal cancer cells stemness via demethylation of stemness genes

Project description:To validate how FIBP influences stemness, we obtained the genome-wide methylation in HCT116-CSCs by an Illumina HumanMethylation450 BeadChip.

2017-09-27 | GSE104271 | 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