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Gene expression profiling of mouse macrophages following IRF2 knockdown

ABSTRACT: Gene expression profiling of mouse macrophages following IRF2 knockdown

PROVIDER: PRJNA418340 | ENA |

REPOSITORIES: ENA

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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

Gene expression profiling of mouse macrophages following long noncoding RNA Malat1 knockdown

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

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Expression Profiling of Primary Human Proerythroblasts (ProEs) After IRF2, IRF6, and MYB shRNA Knockdown

Project description:IRF2, IRF6, and MYB are candidate regulators of human erythropoiesis. We here examine primary CD34+ hematopoietic stem/progenitor cells (HSPCs)-derived erythroid progenitors with control, IRF2, IRF6, or MYB shRNA lentiviral transduction prior to differentiation. Gene expression microarray profiling datasets for MYB shRNA and control shRNA were obtained from Gene Expression Omnibus (GEO) under accession number GSE25678. The data were analyzed together with the datasets obtained in this study. Primary maturing adult erythroblasts were generated ex vivo from CD34+ hematopoietic stem/progenitor cells (HSPCs) using a serum-free two-phase liquid culture system. CD34+ HSPCs were transduced with lentiviruses containing shRNAs against IRF2 or IRF6 gene, selected and differentiated to proerythroblasts (ProEs). Cells were harvested at day 5 of differentiated and total RNA were extracted. This was used to hybridize to Affymetrix expression arrays using the HG-U133 Plus 2.0 platform.

2012-10-05 | E-GEOD-36988 | biostudies-arrayexpress

Expression Profiling of Primary Human Proerythroblasts (ProEs) After IRF2, IRF6, and MYB shRNA Knockdown

2012-10-05 | GSE36988 | GEO

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

2007-09-01 | GSE5907 | 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.

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Differences in gene expression between WT and IRF2 KO cells

Project description:Gasdermin-D (GSDMD) is cleaved by caspase-1/4/11 in response to canonical and non-canonical inflammasome activation. Upon cleavage, GSDMD oligomerizes and forms membrane pores, resulting in IL-1Î² secretion, pyroptotic cell death and inflammatory pathologies including periodic fever syndromes and septic shock â a plague on modern medicine. The transcriptional machinery that drives the expression of GSDMD is unknown. Here we show that IRF2, a member of the interferon-regulatory factor (IRF) family, is essential for the transcriptional activation of GSDMD. A forward genetic screen with ethyl-N-nitrosourea (ENU)-mutagenized mice unequivocally linked IRF2 to inflammasome signaling. Indeed, GSDMD transcript levels were highly attenuated in Irf2â/â macrophages upon Irf2 deficiency in macrophages, endothelial cells, and multiple organs, corresponding to attenuated IL-1Î² secretion and inhibited pyroptosis. Mechanistically, IRF2 binds a previously uncharacterized site within the GSDMD promoter to directly drive GSDMD transcription for execution of pyroptosis in response to canonical and non-canonical inflammasome activation. Our data illuminate a prominent transcriptional mechanism for the expression of GSDMD, a key mediator of inflammatory pathologies.

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