Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ATAC-seq, we found that chromatin accessibility around transcription start sites (TSS) of proinflammatory cytokinse in HSV-1 infected Rpsa-iKO RAW264.7 was significantly reduced
Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA. To further verify the biological function of RPSA, we constructed the RPSA-deficient RAW264.7 macrophage cell line with the inducible CRISPR-Cas9 system, then found that the deletion of RPSA could effectively reduce the expression of proinflammatory cytokines such as IL-1α, IL-1β, IL-6, IL-12 and TNFα induced by HSV-1 infection.
Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the enrichment of P65 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.
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.
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.
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.
Project description:The purpose of this study was to determine what are the effects of TAO3 deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Tao3−/− 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.
Project description:After HSV-1 infection, ribosomal protein RPSA can recognize viral DNA and promotes the expression of proinflammatory cytokines. Through ChIP-seq, we found that the level of H3K4me3 in proinflammatory cytokines(Il1b, Il6, Il12b, etc.) promoter regions was decreased due to Rpsa deficiency.
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.