Project description:To investigate the function of XAF1 in chromatin openning. Wild-type or XAF1 knockout HT29 cells were infected with VSV for 0 or 3 hours,ATAC-seq was performed. Examination of chromatin openness in Wild-type or XAF1 knockout HT29 cells.
Project description:To investigate the function of XAF1 in immune response, we established XAF1 knockout cell lines in which XAF1 gene has been knockout by sgRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of WT or XAF1 knockout HT29 cells with or without VSV infection
Project description:To investigate the function of XAF1 in chromatin openning. Wild-type or XAF1 knockout HT29 cells were infected with VSV for 0 or 3 hours, ChIP-seq was did with H3K27Ac antibody. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications H3K27Ac in HT29 cells.
Project description:Vesicular stomatitis virus (VSV) and rabies and Chandipura viruses belong to the Rhabdovirus family. VSV is a common laboratory virus to study viral evolution and host immune responses to viral infection, and recombinant VSV-based vectors have been widely used for viral oncolysis, vaccination, and gene therapy. Although the tropism of VSV is broad, and its envelope glycoprotein G is often used for pseudotyping other viruses, the host cellular components involved in VSV infection remain unclear. Here, we demonstrate that the host protein leucine-rich repeat-containing G protein-coupled receptor 4 (Lgr4) is essential for VSV and VSV-G pseudotyped lentivirus (VSVG-LV) to infect susceptible cells. Accordingly, Lgr4-deficient mice had dramatically decreased VSV levels in the olfactory bulb. Furthermore, Lgr4 knockdown in RAW 264.7 cells also significantly suppressed VSV infection, and Lgr4 overexpression in RAW 264.7 cells enhanced VSV infection. Interestingly, only VSV infection relied on Lgr4, whereas infections with Newcastle disease virus, influenza A virus (A/WSN/33), and herpes simplex virus were unaffected by Lgr4 status. Of note, assays of virus entry, cell ELISA, immunoprecipitation, and surface plasmon resonance indicated that VSV bound susceptible cells via the Lgr4 extracellular domain. Pretreating cells with an Lgr4 antibody, soluble LGR4 extracellular domain, or R-spondin 1 blocked VSV infection by competitively inhibiting VSV binding to Lgr4. Taken together, the identification of Lgr4 as a VSV-specific host factor provides important insights into understanding VSV entry and its pathogenesis and lays the foundation for VSV-based gene therapy and viral oncolytic therapeutics.
Project description:To investigate the function of ZUFSP in immune response, we established ZUFSP knockout cell lines in which ZUFSP gene has been knockdown by sgRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of WT or ZUFSP knockdown THP1 cells with or without VSV infection
