Gene expression profiling of γ34.5 deleted HSV1 infected Mouse Embryonic Fibroblasts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Tianli Xia
PROVIDER: E-GEOD-43479 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Gene expression analysis of wild type and STING knock-out Mouse Embryonic Fibroblasts (MEFs) infected with γ34.5 deleted HSV1. Genes whose expression that are affected by HSV1 in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated.
2013-01-15 | GSE43479 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-01-15 | E-GEOD-43482 | biostudies-arrayexpress
Project description:IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene. Peritoneal macrophages from WT of IRF3-/- B6 mice were infected with VSV(1 M.O.I. ) for 6 hous, and then subjected to microarray analysis.
2012-05-19 | E-GEOD-37855 | biostudies-arrayexpress
Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.
2014-05-31 | E-GEOD-57603 | biostudies-arrayexpress
Project description:We attempted to identify potential miRNAs that can regulate viral replication by screening host miRNAs in EV71-infected RD cells. To compare the differential expression of miRNAs in EV71-infected cells at different time points, miRNA expression profiles were analyzed using Agilent Human MicroRNA Array chips. At 5 h p.i., the expression levels of most miRNAs in EV71-infected cells were not different from those of mock-infected cells. However, five miRNAs (miR-574-3p, miR-574-5p, miR-181d, miR-197, and miR-939) showed a miRNAs (miR-193a-3p and miR-324-5p) exhibited a increase in expression level in response to EV71 infection at 10 h p.i. RD cells were seeded (2*106 cells) in 10 cm dishes and incubated overnight. The cells were infected with EV71 (strain 2231) on ice at an M.O.I. of 10. After adsorption for 1 h, the virus suspension was replaced with DMEM containing 2% FBS, and the cells were harvested at the indicated times. Total cellular RNA extraction and miRNA microarray analyses were performed using the Agilent Human MicroRNA Array V2 chip, which contains 723 human and 76 viral miRNAs, each with 16 duplicates. Total gene signals were detected and analyzed using the GeneSpring 7.3.1 software and were normalized to the 75th percentile.
2016-07-03 | E-GEOD-75455 | biostudies-arrayexpress
Project description:Gene expression analysis of wild type, STING knock-out and STAT1 knock-out Mouse Embryonic Fibroblasts (MEFs) stimulated with 90-mer dsDNA or 90-mer ssDNA. Genes whose expression that are affected by cytosolic DNA in a STING dependent manner will be identified and signaling pathways regulated by STING will be elucidated. Primary MEFs were mock treated or transfected with dsDNA90 or ssDNA90 for 3 hours. Total RNA was then extracted for array analysis.
2013-01-15 | E-GEOD-43481 | biostudies-arrayexpress
Project description:Hepatitis C virus interacts extensively with host factors not only to establish productive infection but also to trigger unique pathological processes. Our recent genome-wide siRNA screen demonstrated that IKKα is a critical host factor for HCV. Here we describe a novel NF-κB-independent and kinase-mediated nuclear function of IKKα in HCV assembly. HCV infection, through its 3’-untranslated region, interacts with DDX3X to activate IKKα, which translocates to the nucleus and induces a CBP/p300-mediated transcriptional program involving SREBPs. This novel innate pathway induces lipogenic genes and enhances core-associated lipid droplet formation to facilitate viral assembly. Chemical inhibitors of IKKα suppress HCV infection and IKKα-induced lipogenesis, offering a proof-of-concept approach for novel HCV therapeutic development. Our results show that HCV commands a novel mechanism to its advantage by exploiting intrinsic innate response and hijacking lipid metabolism, which likely contributes to a high chronicity rate and the pathological hallmark of steatosis in HCV infection. Cells were treated with either non-targeting control siRNA or siRNA against IKKalpha. After 72 h, cells were either mock infected or infected with HCV JFH-1 strain with the M.O.I. of 0.5.
2013-05-08 | E-GEOD-46528 | biostudies-arrayexpress
Project description:In this study we examined the effects of loss of the MYST histone acetyltransferase TIP60 (KAT5) in mouse embryonic fibroblasts (MEFs), human embryonic kidney cells 293 (HEK293), and human osteosarcoma cells (U2OS) on cell proliferation, BrdU incorporation, cell cycle progression, apoptotic and other forms of cell death, DNA damage, histone acetylation at specific lysine residues and RNA expression levels. This dataset relates to MEFs. To assess the effects of loss of TIP60 on RNA levels, RNA-seq was performed on MEFs, where the TIP60 gene was deleted using Cre/loxP technology. Nuclear translocation was induced with 4-OH-tamoxifen treatment for 3 and 5 days to induce TIP60 gene deletion in the samples also containing the loxP sited in the Tip60 locus.
2022-07-22 | GSE208380 | GEO
Project description:We present a microarray analysis of primary mouse astrocytes exposed to HIV-1 in culture. Results are compared with previous genomic studies of HIV-1 effect in human astrocytes and human and macaque brains. Day-two neonatal mouse astrocytes were exposed in triplicates to cell-free HIV-1/NL4-3 at m.o.i. of 1 and cultured for 24 hours. As control, cells were treated in triplicates with a mock virus concentrate at the same dilution (vol/vol) as the wild-type virus. As an example of large scale gene expression analysis we shall provide some details of the method; full description is in Kim et al. (S.-Y. Kim et al., 2004). Total RNA was prepared from cell cultures using the RNAeasy total RNA extraction kit (Qiagen, CA). RNA quality was assessed by electrophoresis and spectrophotometric analysis; between 1 and 10 µg of total RNA was used to generate a cDNA, and then 1 µg of cDNA product was used in an in vitro transcription reaction that contained biotinylated UTP and CTP. Twenty µg of full-length cRNA was fragmented and was subjected to gene expression analysis on the Affymetrix Mouse Genome 430 2.0 Array chip. Affymetrix software was used to generate CHP files. Significance analysis was performed using ArrayAssist software (Stratagene).
2009-08-05 | E-GEOD-17383 | biostudies-arrayexpress
Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), Trex1 deficient MEFs (TKO) or STING and Trex1 double deficient MEFs (STKO) transfected with or without double strand DNA 90 (ISD) and examined cytokine production by these cells.
2014-07-09 | E-GEOD-59218 | biostudies-arrayexpress