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Genome-wide maps of IRF3 and YAP in gastric cancer cells.

ABSTRACT: We performed chromatin immunoprecipitation (ChIP) assays with YAP and IRF3 antibodies in HGC-27 cells. Analysis of the distribution of YAP- or IRF3-binding sites relative to genes annotated in the human genome, revealed that only a minute fraction of peaks mapped close (<1 kb) to transcription start sites (TSSs) whereas most peaks were located farther than 10 kb from the closest TSS. A total of 6,277 peaks were identified by both YAP and IRF3 antibodies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109081 | GEO | 2021/11/01

REPOSITORIES: GEO

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RNAseq analyze global transcriptome of changes between siIRF3 and siYAP in Gastric cancer cells

Project description:Purpose: To investigate the signal crosstalk between IRF3 and YAP, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by the knockdown of IRF3 or YAP in HGC-27 cells. Methods: Total RNA was extracted from HGC-27 cell after transfection with negative control siRNA (n.c.), IRF3 siRNA (siIRF3) or YAP siRNA (siYAP). Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform. Results: Approximately one thousand transcripts showed differential expression between the siIRF3/siYAP and n.c., with a Fold-change>=2 and q-value <= 0.05. Gene ontology (GO) and gene set enrichment analysis (GSEA) showed a significant negative enrichment of YAP target genes identified by three independent studies in IRF3-knockdown condition. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding the signal crosstalk between IRF3 and YAP.

2018-08-01 | GSE102112 | GEO

RNAseq analyze global transcriptome of changes between siIRF3 and siYAP in Gastric cancer cells

Project description:Purpose: To investigate the signal crosstalk between IRF3 and YAP, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by the knockdown of IRF3 or YAP in HGC-27 cells. Methods: Total RNA was extracted from HGC-27 cell after transfection with negative control siRNA (n.c.), IRF3 siRNA (siIRF3) or YAP siRNA (siYAP). Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform. Results: Approximately approximately one thousand transcripts showed differential expression between the siIRF3/siYAP and n.c., with a Fold-change>=2 and q-value <= 0.05. Gene ontology (GO) and gene set enrichment analysis (GSEA) showed a significant negative enrichment of YAP target genes identified by three independent studies in IRF3-knockdown condition. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding the signal crosstalk between IRF3 and YAP.

2018-01-10 | GSE109028 | GEO

Macropahge-specific Irf3 prevents viral inflammation

Project description:Viral inflammation contributes to pathogenesis and mortality during respiratory virus infections. We recently uncovered Irf3, a critical component of innate antiviral immune responses, interacts with pro-inflammatory transcription factor NF-kB, and inhibits its activity. Irf3, using this mechanism, suppresses inflammatory gene expression in virus-infected cells and mice. In this study, we evaluated the cells responsible for Irf3-mediated suppression of viral inflammation using newly engineered conditional Irf3Δ/Δ mice. Irf3Δ/Δ mice, upon respiratory virus infection, showed increased susceptibility and mortality. Irf3 deficiency caused enhanced inflammatory gene expression, lung inflammation, immunopathology, and damage, which were accompanied by increased infiltration of pro-inflammatory macrophages. Deletion of Irf3 in macrophages (Irf3-MKO) displayed, similar to Irf3Δ/Δ mice, increased inflammatory responses, macrophage infiltration, lung damage, and lethality, indicating Irf3 in these cells suppressed lung inflammation. RNA-seq analyses revealed enhanced NF-kB-dependent gene expression along with activation of inflammatory signaling pathways in infected Irf3MKO lungs. Targeted analyses revealed activated MAPK signaling in Irf3MKO lungs. Therefore, Irf3 inhibited inflammatory signaling pathways in myeloid cellsmacrophages to prevent viral inflammation and pathogenesis.

2024-08-16 | GSE267631 | GEO

Genome-wide binding of transcription factor IRF3

Project description:Genome-wide binding of IRF3 was analysed in MM1.S cells using ChIP-seq high-throughput approach. MM1.S cells were fixed in 1% formaldehyde (Alfa Aesar) for 15min at room temperature. cells were lysed with hypotonic lysis buffer for 15minutes followed by nuclear lysis buffer for 15min on ice. ChIP for IRF3 performed by a standard ChIP-seq protocol and the genome-wide binding of IRF3 data was analysed which revealed peaks enrichment at cell cycle genes TSS.

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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

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

IRF3 and ZBP1

Project description:IRF3 and ZBP1

| PRJNA686391 | ENA

Gene expression in IRF3-/- peritoneal macrophage infected with VSV

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2012-05-19 | E-GEOD-37855 | biostudies-arrayexpress

IRF3 drives replication stress signaling and determines sensitivity to genotoxic agents in triple-negative breast cancer cells

Project description:Interferon-β signaling has been shown to play important roles in anti-virus as well as anti-tumor immunity. We here report that the key transcription factor in type I interferon signaling, IRF3, as well as downstream interferon-β are able to induce replication stress signaling in triple-negative breast cancer cells. IRF3 overexpression sensitizes triple-negative breast cancer cells to several genotoxic agents. Addition of IFN-β, a key downstream cytokine of IRF3,reduced replication fork speed and activated ATR-CHK1 signaling. Conversely, type I interferon-neutralizing antibodies or nucleosides supplementation rescued IRF3-induced replication stress.

2024-05-01 | GSE263947 | GEO

The IRF3 dependent response of macrophages to M. tuberculosis infection

Project description:Transcriptional profiling of macrophages (wild-type and IRF3-/- ) infected with various M.tuberculosis strains (wild-type and ESX-1 mutant) Comparison of the global gene expression of wild-type BMDM macrophages and IRF3-/- macrophages infected with either wild-type M.tuberculosis or ESX-1 mutant M.tuberculosis, with two biological replicates per group

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