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Next Generation Sequencing and Analysis of the Transcriptomes of RAW264.7 cells pretreated with PEP and PBS.

ABSTRACT: We demonstrate that phosphoenolpyruvate (PEP) generally inhibits viral infection in vitro and in vivo. In order to further explore whether PEP controls viral replication through a general mechanism such as enhancing innate response, and if not, what's the critical downstream target(s) of PEP, we performed RNA sequencing (RNA-seq) analysis on the RAW264.7 cells that were pretreated with 250 μM PEP or PBS for 2 hours, and then infected with or without vesicular stomatitis virus (VSV) for 8 hours.

ORGANISM(S): Mus musculus

PROVIDER: GSE223228 | GEO | 2023/03/16

REPOSITORIES: GEO

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Next Generation Sequencing Analysis of the Transcriptomes of Wild Type and ALKBH5-/- Peritoneal Macrophages

Project description:By performing RNA sequencing (RNA-seq) analysis on the peritoneal macrophages that derived from ALKBH5-/- mice and littermate mice infected with or without vesicular stomatitis virus (VSV), we want to investigate whether deficiency of ALKBH5 controls viral replication through a more general mechanism such as enhancing innate response, and if not, what's the critical downstream target(s) of ALKBH5. RNA-seq analysis showed that mRNA expression of innate genes remained unchanged or not increased in ALKBH5-deficient cells. While thourgh KEGG pathway enrichment analysis of the RNA-seq data, we found that metabolic pathways were the ones most significantly affected in ALKBH5-deficient macrophages upon VSV infection. These results demonstrated that deficiency of ALKBH5 controls viral replication by significantly changing the metabolism-related genes expression.

2019-08-22 | GSE127739 | GEO

Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection.

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody (Abcam, ab4729). We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

2022-06-29 | GSE133784 | GEO

Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody. We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

2018-07-07 | GSE116750 | GEO

WT and IFN-I receptor deficient mouse macropahge expression profiling under virus infection or under IFNb stimulation

Project description:To investigate the role of lncRNAs in viral infection and their relationship with the IFN-I system, we profiled lncRNA expression in wild type (WT) and IFN-I receptor deficient (Ifnar-/-) cells infected with or without vesicular stomatitis virus (VSV).

2017-12-14 | GSE102179 | GEO

Mouse macropahge RNA-seq with or without virus infection

2017-12-14 | GSE100873 | GEO

UV cross-linking RIP-seq of VSV-GFP-infected HEK293T cells overexpressed PTENα

Project description:To determine whether PTENα directly binds to viral RNA or host mRNA, we performed UV cross-linking RNA immunoprecipitation (RIP) sequencing of HEK293T cells transfected with vector encoding PTENα under VSV-GFP (green fluorescent protein-expressing vesicular stomatitis virus) infection

2024-02-19 | GSE218439 | GEO

HyperTRIBE assay of VSV-GFP-infected HEK293T cells overexpressing ADAR1-CD, PTENα-N(WT)-ADAR1-CD, or PTENα-N(6R/D)-ADAR1-CD fusion protein

Project description:To explore the binding sites of PTENα on viral or host RNAs, we performed HyperTRIBE assay of HEK293T cells overexpressing ADAR1-CD, PTENα-N(WT)-ADAR1-CD, or PTENα-N(6R/D)-ADAR1-CD fusion protein under VSV-GFP (green fluorescent protein-expressing vesicular stomatitis virus) infection.

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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

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

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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