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Article: RIOK3 is an adaptor protein required for IRF3-mediated antiviral type I interferon production

TitleRIOK3 is an adaptor protein required for IRF3-mediated antiviral type I interferon production
Authors
Issue Date2014
Citation
Journal of Virology, 2014, v. 88, n. 14, p. 7987-7997 How to Cite?
AbstractDetection of cytosolic nucleic acids by pattern recognition receptors leads to the induction of type I interferons (IFNs) and elicits the innate immune response. We report here the identification of RIOK3 as a novel adaptor protein that is essential for the cytosolic nucleic acid-induced type I IFN production and for the antiviral response to gammaherpesvirus through two independent kinome-wide RNA interference screens. RIOK3 knockdown blocks both cytosolic double-stranded B-form DNA and doublestranded RNA-induced IRF3 activation and IFN-β production. In contrast, the overexpression of RIOK3 activates IRF3 and induces IFN-β. RIOK3 functions downstream of TBK1 and upstream of IRF3 activation. Furthermore, RIOK3 physically interacts with both IRF3 and TBK1 and is necessary for the interaction between TBK1 and IRF3. In addition, global transcriptome analysis shows that the expression of many gene involved antiviral responses is dependent on RIOK3. Thus, knockdown of RIOK3 inhibits cellular antiviral responses against both DNA and RNA viruses (herpesvirus and influenza A virus). Our data suggest that RIOK3 plays a critical role in the antiviral type I IFN pathway by bridging TBK1 and IRF3. © 2014, American Society for Microbiology.
Persistent Identifierhttp://hdl.handle.net/10722/285744
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFeng, Jun-
dc.contributor.authorDe Jesus, Paul D.-
dc.contributor.authorSu, Victoria-
dc.contributor.authorHan, Stephanie-
dc.contributor.authorGong, Danyang-
dc.contributor.authorWu, Nicholas C.-
dc.contributor.authorTian, Yuan-
dc.contributor.authorLi, Xudong-
dc.contributor.authorWu, Ting Ting-
dc.contributor.authorChanda, Sumit K.-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:31Z-
dc.date.available2020-08-18T04:56:31Z-
dc.date.issued2014-
dc.identifier.citationJournal of Virology, 2014, v. 88, n. 14, p. 7987-7997-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285744-
dc.description.abstractDetection of cytosolic nucleic acids by pattern recognition receptors leads to the induction of type I interferons (IFNs) and elicits the innate immune response. We report here the identification of RIOK3 as a novel adaptor protein that is essential for the cytosolic nucleic acid-induced type I IFN production and for the antiviral response to gammaherpesvirus through two independent kinome-wide RNA interference screens. RIOK3 knockdown blocks both cytosolic double-stranded B-form DNA and doublestranded RNA-induced IRF3 activation and IFN-β production. In contrast, the overexpression of RIOK3 activates IRF3 and induces IFN-β. RIOK3 functions downstream of TBK1 and upstream of IRF3 activation. Furthermore, RIOK3 physically interacts with both IRF3 and TBK1 and is necessary for the interaction between TBK1 and IRF3. In addition, global transcriptome analysis shows that the expression of many gene involved antiviral responses is dependent on RIOK3. Thus, knockdown of RIOK3 inhibits cellular antiviral responses against both DNA and RNA viruses (herpesvirus and influenza A virus). Our data suggest that RIOK3 plays a critical role in the antiviral type I IFN pathway by bridging TBK1 and IRF3. © 2014, American Society for Microbiology.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleRIOK3 is an adaptor protein required for IRF3-mediated antiviral type I interferon production-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.00643-14-
dc.identifier.pmid24807708-
dc.identifier.pmcidPMC4097797-
dc.identifier.scopuseid_2-s2.0-84904191854-
dc.identifier.volume88-
dc.identifier.issue14-
dc.identifier.spage7987-
dc.identifier.epage7997-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000338442600029-
dc.identifier.issnl0022-538X-

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