ArticleJournal of virology2005
Analysis of genes induced by Sendai virus infection of mutant cell lines reveals essential roles of interferon regulatory factor 3, NF-kappaB, and interferon but not toll-like receptor 3.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 109 citations in OpenAlex.
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- SAMHD1 suppresses innate immune responses to viral infections and inflammatory stimuli by inhibiting the NF-κB and interferon pathways.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Quantitative profiling of innate immune activation by viral infection in single cells.Integrative biology : quantitative biosciences from nano to macro · 2017Article
- Type I Interferon-Mediated Induction of Antiviral Genes and Proteins Fails to Protect Cells from the Cytopathic Effects of Sendai Virus Infection.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016Article
- Rapid induction and persistence of paracrine-induced cellular antiviral states arrest viral infection spread in A549 cells.Virology · 2016Article
- Robust Lys63-Linked Ubiquitination of RIG-I Promotes Cytokine Eruption in Early Influenza B Virus Infection.Journal of virology · 2016Article
- Characterization of a Novel Human-Specific STING Agonist that Elicits Antiviral Activity Against Emerging Alphaviruses.PLoS pathogens · 2015Article
- Limited specificity of IRF3 and ISGF3 in the transcriptional innate-immune response to double-stranded RNA.Journal of leukocyte biology · 2015Article
- Interferon-induced Ifit proteins: their role in viral pathogenesis.Journal of virology · 2015Review
- Genome rearrangement affects RNA virus adaptability on prostate cancer cells.Frontiers in genetics · 2015Article
- The human cytomegalovirus UL26 protein antagonizes NF-κB activation.Journal of virology · 2014Article
- Visualizing infection spread: dual-color fluorescent reporting of virus-host interactions.Biotechnology and bioengineering · 2014Article
- dsRNA-activation of TLR3 and RLR signaling: gene induction-dependent and independent effects.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- dsRNA-dependent protein kinase PKR and its role in stress, signaling and HCV infection.Viruses · 2012Review
- TRIM56 is an essential component of the TLR3 antiviral signaling pathway.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Sendai virus (SeV) infection causes the transcriptional induction of many cellular genes that are also induced by interferon (IFN) or double-stranded RNA (dsRNA). We took advantage of various mutant cell lines to investigate the putative roles of the components of the IFN and dsRNA signaling pathways in the induction of those genes by SeV. Profiling the patterns of gene expression in SeV-infected cells demonstrated that Toll-like receptor 3, although essential for gene induction by dsRNA, was dispensable for gene induction by SeV. In contrast, Jak1, which mediates IFN signaling, was required for the induction of a small subset of genes by SeV. NF-kappaB and interferon regulatory factor 3 (IRF-3), the two major transcription factors activated by virus infection, were essential for the induction of two sets of genes by SeV. As expected, some of the IRF-3-dependent genes, such as ISG56, were more strongly induced by SeV in IRF-3-overexpressing cells. Surprisingly, in those cells, a number of NF-kappaB-dependent genes, such as the A20 gene, were induced poorly. Using a series of cell lines expressing increasing levels of IRF-3, we demonstrated that the degree of induction of A20 mRNA, upon SeV infection, was inversely proportional to the cellular level of IRF-3, whereas that of ISG56 mRNA was directly proportional. Thus, IRF-3 can suppress the expression of NF-kappaB-dependent genes in SeV-infected cells.
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