Project description:Analysis of gene expression in macrophages infected with influenza A virus or non-infected and treated with the saliphenylhalamide, obatoclax, expressing wild type NS1 protein or its mutant R38A, K41A. The hypothesis tested was that R38 and K41 residues within viral NS1 protein are essential for transctiptional control of cellluar gene expression. Cells were infected with influenza A/WSN/33 viruses expressing wild type NS1 protein (WT), its R38A, K41A mutant (RK/AA) or non-infected (Mock)
Project description:Proteomic data from dengue virus infected U-937 cells. PVD_C samples were infected via antibody-mediated or DC-SIGN receptor mediated entry routes with wild-type DENV-4 or mock inoculum; time points 2, 8, 16, and 24 hours; 5 biological replicates. PVD_L samples were infected via antibody-mediated or DC-SIGN receptor mediated entry routes with wild-type DENV-1 or mock inoculum; time points 2, 6, 10, 18, 24, and 30 hours; 5 biological replicates.
Project description:To investigate the repertoire of proteins interacting with the Aedes aegypti TUDOR protein AAEL012437 (Veneno), we transiently expressed a GFP-Veneno transgene in Aag2 cells. These cells were either infected with the alphavirus Sindbis virus (SINV) or mock-infected. Subsequently, cells were lysed and processed for immunoprecipitation using GFP-TRAP beads to purify Veneno-complexes. The same approach was followed for a truncated transgene lacking the first 205 amino acids (C206).
Project description:MicroRNA-203 was up-regulated markedly upon H5N1 virus infection. To identify the potential target genes of miR-203, we constructed a miR-203 knockout A549 cell line. Then wild-type and miR-203 knockout A549 cells were mock-infected or infected with H5N1 virus for 48h. The Agilent Whole Human Genome Oligo Microarray was performed to analyze the mRNA expression profiling. Meanwhile, the online tool TargetScanHuman (http://www.targetscan.org/vert_71/) was used to predict biological targets of miR-203. We combined the predicted genes with the genes differentially expressed in wild-type and miR-203 knockout A549 cells, and preliminarily identified some candidate mRNAs. Then more experiments were performed to further verify these target genes, such as dual-luciferase reporter assay, quantitative real-time PCR or Western blot analysis.
Project description:Gene expression analysis of tumors isolated from mice after they received treatments with Sindbis Virus vectors for 1 week. The hypothesis tested changes in the transcriptome profiles of tumors isolated from Sindbis virus vectors treated and untreated mice. Expression profiling by high throughput sequencing of MOSEC.Fluc.p11 tumors
Project description:To investigate how murine airway epithelial cells respond to Influenza infection and how important interferon type I signaling is for this response, we harvested airway epithelial cells from the tracheas of wild type, interferon type I knockout(IFNaR-/-) and STAT1 knockout (STAT1-/-) mice and cultured them as previously described (Pickles et al,1998) in polarized airway epithelial cell cultures (mAECs). Triplicate mAECs from each type of mouse (wt,IFNaR-/-,STAT1-/-) were infected with 2X105 PFUs Influenza A (WSN) for 2h or mock inoculated and harvested 24h after infection. Triplicate murine polarized airway epithelial cell cultures from wild type, IFNaR-/- or STAT1-/- mice were mock treated or infected with 2x10^5 PFUs of Influenza A (WSN) for 2h and harvested 24 h post infection.
Project description:We performed Fluidigm C1 single cell sequencing analysis of wild-type and microRNA deficient (Dgcr8 knockout) mouse embryonic stem cells mock treated or transfected with either miR-294 or let-7.
Project description:Analysis of gene expression in macrophages infected with influenza A virus or non-infected and treated with the saliphenylhalamide, obatoclax, expressing wild type NS1 protein or its mutant R38A, K41A. The hypothesis tested was that R38 and K41 residues within viral NS1 protein are essential for transctiptional control of cellluar gene expression. Cells were infected with influenza A/WSN/33 viruses expressing wild type NS1 protein (WT), its R38A, K41A mutant (RK/AA) or non-infected (Mock) Total RNA isolated from macrophages 8 hours post stimuation.