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Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

ABSTRACT: To investigate the role of the IRF family in the regulation of interferon stimulated genes, we conducted CRISPR/Cas9 mediated genome editing of Irf3, Irf7 or Irf9 in sgScd2 Th1 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of control, sgScd2, sgScd2/sgIrf3, sgScd2/sgIrf7 or sgScd2/sgIrf9 Th1 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE200636 | GEO | 2022/08/03

REPOSITORIES: GEO

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Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

Project description:Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

| PRJNA825571 | ENA

Specificity of enhancer selection by IRF3, IRF5 and IRF9 in dendritic cells

Project description:To discover the key determinants of IRF-specific enhancer selection, we identified and characterized IRF binding regions. Using chromatin immunoprecipitation coupled with deep sequencing (ChIP-seq), we mapped the binding regions of IRF3, IRF5, and IRF9 in murine dendritic cells (DCs) stimulated with TLR3 and TLR9 agonists, as well as IFNβ, respectively. We comprehensively analysed the IRF cistromes to identify characteristic features, including DNA motifs for IRFs and other transcription factors, and chromatin status.

2019-07-31 | GSE125340 | GEO

Genome-wide RNA-seq transcriptional analysis of splenocyte responses to Dengue virus infection in WT, Irf3(-/-)×Irf7(-/-) (DKO), Irf3-/-xIrf5-/-xIrf7-/- (TKO), and Ifnar1-/- (AB6) mice.

Project description:Interferon-regulatory factors (IRFs) are a family of transcription factors (TFs) that play critical roles in translating viral recognition into antiviral responses, including type I IFN production. Dengue virus (DENV) and other clinically important flaviviruses are controlled by functional type I interferon (IFN) responses. Using an experimental model of DENV infection that recapitulates key aspects of the human disease in mice, we demonstrate that while mice lacking the type I IFN receptor (Ifnar1-/-) succumb to DENV infection, mice that are deficient in IRF-3, IRF-5, and IRF-7 – the three transcription factors thought to regulate type I IFN production – survive DENV challenge. Genome-wide RNA-seq analysis of WT, Irf3(-/-)×Irf7(-/-) (DKO), Irf3-/-xIrf5-/-xIrf7-/- (TKO), and Ifnar1-/- (AB6) splenocytes identified minimal type I IFN production but a robust type II IFN (IFN-γ) response in DKO and TKO mice later shown to be dependent on IRF-1. These results reveal a key role for IRF-1 in antiviral defense by activating both type I and II IFN responses during DENV infection.

2017-11-07 | GSE104189 | GEO

Irf3 phenotyping

Project description:The interferon regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to influenza A virus infections in Irf3-/-, Irf7-/- and Irf3-/-Irf7-/- knock-out mice.

2016-11-02 | GSE77600 | GEO

DNA-binding of IRF3, IRF5 and IRF7 transcription factors

Project description:DNA-binding of IRF3, IRF5 and IRF7 transcription factors

| PRJNA429664 | ENA

Investigation of genome wide binding profile of IRF9 in I-IFN treated or sgScd2 Th1 cells

Project description:To investigate the role of IRF9 in the transcriptional regulation of interferon stimulated genes in sgScd2 Th1 cells, we assessed the genome-wide binding pattern of IRF9 by chromatin immunoprecipitation DNA-sequencing (ChIP-seq).

2022-08-03 | GSE200625 | GEO

Transcription profiling of skin from interferon regulatory factor 6 (Irf6) knockout mice and wild type mice to study the role for Irf6 in epidermal development.

Project description:Transcription factor paralogs may share a common role (e.g. Hox) in staged or overlapping expression in specific tissues. In other examples, members have distinct roles in a range of embryologic, differentiation or response pathways (e.g. Tbx, Pax). For the Interferon Regulatory Factor (IRF) family of transcription factors, mice deficient in Irf1, Irf2, Irf3, Irf4, Irf5, Irf7, Irf8 or Irf9, have defects in the immune response but display no embryologic abnormalities. Mice deficient for Irf6 have not been reported, but in humans, mutations in IRF6 cause two Mendelian orofacial clefting syndrome, and genetic variation in IRF6 confers risk for isolated cleft lip and palate. Mice deficient for Irf6 have abnormal skin, limb and craniofacial development. Histological and gene expression analyses indicate that the primary defect is in keratinocyte differentiation and proliferation. This study describes a novel role for an IRF family member in epidermal development. Experiment Overall Design: Skin from E17.5 mice was removed and flash frozen for RNA extraction and hybridization on Affymetrix microarrays.

2007-11-13 | E-GEOD-5800 | biostudies-arrayexpress

DNA-binding of IRF3, IRF5 and IRF7 transcription factors

Project description:The Interferon Regulatory Factors (IRFs) are essential regulators of the innate immune response to viruses. IRFs 3, 5, and 7 drive type-1-interferon and cytokine production in a cell-type and stimulus-specific manner, suggesting regulatory complexity. IRFs 3, 5 and 7 bind DNA as phosphorylation-activated dimers and are classically described as binding a doublet of the canonical IRF binding site: 5'-AANNGAAA-3’. IRF3/5/7 have both common and distinct gene targets and the simple canonical motif does not capture the regulatory complexity of IRF-dependent gene expression. Previous studies, both low and high throughput, have refined our understanding of IRF regulation, yet a systematic comparison of DNA binding preferences for active, dimeric IRF complexes has not been performed. To address this, we designed an IRF-specific, custom protein-binding microarray (PBM) that includes synthetic IRF binding sites as well as type-1-interferon and cytokine promoters. Using constitutively active, phosphomimetic IRF3, 5 and 7 dimers, we find key DNA binding differences for these factors with implications for IRF-dependent gene regulation.

2018-01-12 | GSE109117 | GEO

Transcriptomic profiling of bat PakiT03 cells with immune stimulation

Project description:To examine innate immune signalling, IFN baseline and IRF-regulation, we profile Pteropus alecto bat kidney epithelial cells (PakiT03) with Deep NGS coverage. Clonal cell lines were also isolated with CrispR KO for IRF1, IRF3, IRF7, IFNAR2 or IFNAR2/IRF7 double KO.

2020-03-29 | GSE129390 | GEO

Characterising the transcriptional profile of murine 3T3-L1 adipocytes with altered expression of IRF3.

Project description:The chronic inflammatory state that accompanies obesity is a major contributor to insulin resistance and other metabolic dysfunction features. Despite recent advances in our understanding of the cellular and secreted factors that promote the inflammatory milieu of obesity, we have much less insight into the transcriptional pathways that drive these processes. While most attention has focused on the canonical inflammatory transcription factor NF-KB, other potentially important factors exist, including members of the interferon regultory factor (IRF) family. Here we show that IRF3 expression is upregulated in the adipocytes of obese mice and humans. TLR3/TLR4 activation induces insulin resistance in adipocytes, which can be prevented by IRF3 knockdown. Furthermore, Irf3KO mice display improved insulin sensitivity, associated with reduced intra-adipose and systemic inflammation in the high-fat fed state, enhanced browning of subcutaneous fat, and increased adipose expression of Glut4. Taken together, our data indicates that IRF3 is a major transcriptional regulator of adipose inflammation to maintain systemic glucose and energy homeostasis. Transcriptional profiling of murine 3T3-L1 adipocytes with altered expression of IRF3. Overexpression or knockdown of IRF3 was achieved by lentivirus transduction for 6 days. 3T3-L1 adipocytes with IRF3 knockdown were further treated in the absence or presence of LPS for 6 days. Samples consist of triplicate replica with appropriate control.

2016-05-31 | E-GEOD-81193 | biostudies-arrayexpress

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