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

ABSTRACT: IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene.

ORGANISM(S): Mus musculus

PROVIDER: GSE37855 | GEO | 2012/05/20

SECONDARY ACCESSION(S): PRJNA163895

REPOSITORIES: GEO

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

Project description:IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene. Peritoneal macrophages from WT of IRF3-/- B6 mice were infected with VSV(1 M.O.I. ) for 6 hous, and then subjected to microarray analysis.

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

miRNA profiling of mouse primary peritoneal macrophages infected with vesicular stomatitis virus (VSV)

Project description:To investigate whether and what miRNAs expression might be regulated by VSV (vesicular stomatitis virus?) challenge, we analyzed the miRNA expression profile of mouse primary peritoneal macrophages infected with VSV by using an array-based miRNA profiling. After the infection of VSV at MOI 10 for 48 h, the array revealed that many miRNAs were up-regulated in macrophages?

2009-05-11 | E-MEXP-2110 | biostudies-arrayexpress

Gene expression from splenic cells in response to VSV-M2 and ligands to RIG-I and MDA5

Project description:VSV-M2 is recognized by cytosolic RIG-I. Notably, 5'-triphosphate RNA molecules derived from either viral RNA or from the synthetically produced 3pRNA can also induce RIG-I activation. MDA5 stimulation is achieved using complexed poly(I:C), a synthetic analog of viral dsRNA. To test whether the RIG-I and MDA5 ligands 3pRNA and poly(I:C) can be used in their complexed structures to decipher RNA virus-induced sickness behavior in vivo, we first compared the tissue-specific signaling pathways after systemic challenge with VSV-M2 and the RIG-I and MDA5 ligands, respectively. A whole-genome expression analysis using splenic cells was carried out using an Affymetrix Mouse Gene 2.1 ST Array.

2016-04-20 | GSE74015 | 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

Gene expression in HeLa cells expressing GFP-IRF3 (non-targeting control and clonal knockouts of DDX58, MAVS, ATP13A1, CAPN15, TADA2B, MED16, and MED24) following Sendai virus (SeV) infection or hpRNA transfection

Project description:IRF3 translocates from the cytoplasm to the nucleus upon recognition of a cytoplasmic RNA stimulus by RIG-I or MDA5. Using an optical pooled CRISPR knockout screen in HeLa-Cas9 cells, we identified ATP13A1, CAPN15, TADA2B, MED16, and MED24 as novel genes affecting the translocation of IRF3 upon Sendai virus infection. We generated isogenic clonal knockout HeLa-Cas9 lines and confirmed that loss of these five novel genes results in either decreased (ATP13A1 and CAPN15) or increased (TADA2B, MED16, and MED24) translocation of IRF3 upon Sendai virus or synthetic hpRNA stimulation.

2023-03-05 | GSE179288 | GEO

RNA transcriptome analysis of IRF1 and IRF3 knockout in immortalized primary hepatocytes infected with hepatitis A virus

Project description:Interferon regulatory factors (IRFs) play key roles in the transactivation of antiviral genes at the step downstream of activated pathogen-associated molecular pattern sensors, such as RIG-I-like receptors or Toll-like receptors. Whereas IRF1 and IRF3 are thought to bind similar DNA elements (ISRE and PRD-III, PRD-I) to activate antiviral gene transcription, genome-wide transcriptome profiling of IRF1 versus IRF3 knockouts in an immortalized primary hepatocyte (PH5CH8) cell line infected with hepatitis A virus (HAV) revealed unexpected disparities in their target genes. IRF1 targets include several anti-HAV effector genes that were not previously recognized to have antiviral functions.

2018-06-01 | GSE114916 | GEO

Gene expression in RAW264.7 cells infected with VSV and HSV-1

Project description:The purpose of this study was to determine which genes are differentially regulated virus infection in RAW264.7 cells. Cells were infected with Vesicular Stomatitis Virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed, focusing on F-box proteins and E3 ubiquitin ligases. RAW264.7 cells were infected with Vesicular Stomatitis Virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.

2016-04-05 | E-GEOD-72077 | biostudies-arrayexpress

Gene expression in Src-/- RAW264.7 cells infected with VSV and HSV-1

Project description:The purpose of this study was to determine what are the effects of Src deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.

2016-07-01 | E-GEOD-81675 | biostudies-arrayexpress

Expression data from mouse peritoneal macrophages

Project description:Biologic functions involved in innate immune response of macrophages rely on the precise regulation of kinds of immune molecular. In the virus infection procession, the macrophages are activated following a tightly controlled genetic programme where specific sets of genes are up-regulated or down-regulated. We used microarrays to detail the global programme of gene expression underlying VSV infection and identified distinct classes of up-regulated and down-regulated genes during this process. Mouse peritoneal macrophages were selected with/without VSV infection for 8 hours for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain expression profiles. We selected macrophages according to VSV infection at two time-points: uninfected macrophage(control) and VSV infected for 8 hour macrophages(VSV).

2012-07-23 | E-GEOD-39620 | biostudies-arrayexpress

Small molecule RIG-I agonist serves to adjuvant broad, multifaceted influenza virus vaccine immunity

Project description:We identified a small molecule compound, KIN1148, that directly binds RIG-I to drive IRF3 and NF B activation and expression of innate immune genes, cytokines and chemokines. KIN1148 activates RIG-I in an RNA- and ATP-independent manner and does not induce a canonical antiviral interferon (IFN) gene program traditionally associated with RIG-I activation. When administered in combination with a vaccine against influenza A virus (IAV), KIN1148 induces both neutralizing antibody and broadly cross-protective IAV-specific T cell responses compared to vaccination alone, which induces poor responses. In this study, we demonstrate that KIN1148 directly engages RIG-I to activate IRF3- and NFB-dependent innate immune responses, making it the first small molecule RIG-I agonist to be identified. Biochemical studies show that KIN1148 binds to RIG-I to drive RIG-I self-oligomerization and downstream signaling activation in an RNA- and ATP-independent manner. We further find that transcriptional programs induced by KIN1148 treatment exhibit shared and unique signatures to that induced by other methods of RIG-I activation, including Sendai virus (SeV) infection and PAMP RNA transfection. KIN1148 adjuvants a split virus (SV) vaccine at suboptimal dose to protect mice from lethal challenge with a recombinant highly pathogenic avian H5N1 influenza virus, A/Vietnam/1203/2004.

2022-06-14 | GSE205964 | GEO

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