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Expression data from C57BL/6J and C57BL6/J Sarm-deficient mice uninfected or infected with vesicular stomatitis virus (VSV)

ABSTRACT: Sarm-deficient mice are protected from VSV encephalitis and death. Microarray was done to examine genes contributing to this phenotype

ORGANISM(S): Mus musculus

PROVIDER: GSE44331 | GEO | 2013/04/04

SECONDARY ACCESSION(S): PRJNA196164

REPOSITORIES: GEO

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Expression data from C57BL/6J and C57BL6/J Sarm-deficient mice uninfected or infected with vesicular stomatitis virus (VSV)

Project description:Sarm-deficient mice are protected from VSV encephalitis and death. Microarray was done to examine genes contributing to this phenotype WT and KO mice were infected with VSV and brains were harvested at day 5 post-infection for RNA extraction

2013-04-04 | E-GEOD-44331 | 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

Transcription profiling of human astrocytes infected with VSV (vesicular stomatitis virus) for 7 days vs. control

Project description:Infected and Uninfected with VSV

2008-06-12 | E-GEOD-2449 | biostudies-arrayexpress

mRNA-seq of immortailized bone marrow derived macrophages (iBMDM) after vesicular stomatitis virus (VSV) infection

Project description:Analysis of mRNA-seq reveals how wild type immortalized bone marrow derived macrophages response to VSV infection

2018-10-02 | GSE120694 | GEO

Vesicular stomatitis virus

Project description:Vesicular stomatitis virus (VSV): Genome sequencing and assembly

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Oncotargeting by Vesicular Stomatitis Virus (VSV): Advances in Cancer Therapy.

Project description: Not available

| S-EPMC5850397 | biostudies-literature

Differential RNA Interactions with Heterogeneous Nuclear Ribonucleoproteins During Vesicular Stomatitis Virus Infection

Project description:Heterogeneous nuclear ribonucleoproteins (hnRNPs) are involved in many processes in RNA metabolism. In addition to their functions in the nucleus, hnRNPs can function in the replication of RNA viruses in the cytoplasm. In vesicular stomatitis virus (VSV)-infected cells, several hnRNPs relocalize from the nucleus to the cytoplasm. This raises the question of whether these hnRNPs are relocalized together with their host nuclear RNAs or whether they associate with new RNAs in the cytoplasm. hnRNP A1, hnRNP C1/C2, and hnRNP K were immunoprecipitated from mock- or VSV-infected cells, and RNAs were analyzed by high content RNA sequencing. Each hnRNP displayed a loss of interaction with cellular transcripts in favor of viral mRNAs. hnRNP A1 was preferentially associated with VSV phosphoprotein (P) mRNA; hnRNP C1/C2 was preferentially associated with VSV glycoprotein (G) mRNA, and hnRNP K bound viral transcripts in rank of abundance.

2016-06-04 | GSE82226 | GEO

Enhanced immunosurveillance for animal morbilliviruses using vesicular stomatitis virus (VSV) pseudotypes.

Project description: Not available

| S-EPMC5084683 | biostudies-literature

Whole genome RNA-seq analysis of wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM), with or without vesicular stomatitis virus (VSV) infection

Project description:Wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM) were infected with VSV for 6h, followed by whole genome RNA-seq analysis. Conclusions: HIPK2 deficiency aggravates viral infection and inhibited the production of IFNβ.

2017-12-15 | GSE108080 | GEO

Analysis of global gene expression profiles of hPAF1 deficient A549 cells during infection with H1N1 influenza A virus or vesicular stomatitis virus (VSV)

Project description:Viral infection is commonly associated with virus-driven hijacking of host proteins. We describe a novel mechanism by which influenza virus impacts host cells through the interaction of influenza NS1 protein with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 targets the transcription elongation PAF1 complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C results in suppression of hPAF1C-mediated transcriptional elongation. More importantly,in the following data sets, we show that hPAF1 plays a crucial role in the antiviral response. Loss of hPAF1C reduces antiviral gene expression and reduces inducible transcription of target genes after stimulation with viral RNA analogue poly(I:C), vesicular stomatitis virus (VSV), exogenous recombinant IFN(beta) and influenza virus (H1N1). This study underscores the importance of hPAF1C in controlling inducible antiviral gene expression. Untreated (no siRNA), control siRNA-treated and hPAF1 siRNA-treated A549 cells were stimulated with A/Puerto Rico/8/1934 influenza virus (H1N1) or vesicular stomatitis virus (VSV). Total RNA was isolated with the Qiagen RNeasy mini kit. 200ng of total RNA per sample was used to prepare biotin-labeled RNA using MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems) and hybridized to HumanHT-12 v4 Expression BeadChips (Illumina). Data analysis was performed using the GeneSpring GX11.0 software (Agilent Technologies). 3 biological replicates per condition

2012-02-15 | E-GEOD-35266 | biostudies-arrayexpress

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