REUL Is a Novel E3 Ubiquitin Ligase and Stimulator of Retinoic-Acid-Inducible Gene-I 英文参考文献.docVIP

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REUL Is a Novel E3 Ubiquitin Ligase and Stimulator of Retinoic-Acid-Inducible Gene-I 英文参考文献.doc

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REUL Is a Novel E3 Ubiquitin Ligase and Stimulator of Retinoic-Acid-Inducible Gene-I 英文参考文献

REULIsaNovelE3UbiquitinLigaseandStimulatorof Retinoic-Acid-InducibleGene-I DongGao,Yong-KangYang,Rui-PengWang,XiangZhou,Fei-CiDiao,Min-DianLi,Zhong-HeZhai, Zheng-FanJiang,Dan-YingChen* KeyLaboratoryofCellProliferationandDifferentiation(MinistryofEducation),CollegeofLifeSciences,PekingUniversity,Beijing,China Abstract RIG-I and MDA5 are cytoplasmic sensors that recognize different species of viral RNAs, leads to activation of the transcriptionfactorsIRF3andNF-kB,whichcollaboratetoinducetypeIinterferons.Inthisstudy,weidentifiedREUL,aRING- fingerprotein,asaspecificRIG-I-interactingprotein.REULwasassociatedwithRIG-I,butnotMDA5,throughitsPRYand SPRY domains. Overexpression of REUL potently potentiated RIG-I-, but not MDA5-mediated downstream signalling and antiviral activity. In contrast, the RING domain deletion mutant of REUL suppressed Sendai virus (SV)-induced, but not cytoplasmicpolyI:C-inducedactivationofIFN-bpromoter.KnockdownofendogenousREULbyRNAiinhibitedSV-triggered IFN-bexpression,andalsoincreasedVSVreplication.Full-lengthRIG-I,butnottheCARDdomaindeletionmutantofRIG-I, underwentubiquitinationinducedbyREUL.TheLys154,164,and172residuesoftheRIG-ICARDdomainwerecriticalfor efficientREUL-mediatedubiquitination,aswellastheabilityofRIG-ItoinduceactivationofIFN-bpromoter.Thesefindings suggestthatREULisanE3ubiquitinligaseofRIG-IandspecificallystimulatesRIG-I-mediatedinnateantiviralactivity. Citation:GaoD,YangY-K,WangR-P,ZhouX,DiaoF-C,etal.(2009)REULIsaNovelE3UbiquitinLigaseandStimulatorofRetinoic-Acid-InducibleGene-I.PLoS ONE4(6):e5760.doi:10.1371/journal.pone.0005760 Editor:Je′romeNigou,InstitutdePharmacologieetdeBiologieStructuraleCNRS205,France ReceivedJanuary3,2009;AcceptedMay6,2009;PublishedJune1,2009 Copyright:?2009Gaoetal.Thisisanopen-accessarticledistributedunderthetermsoftheCreativeCommonsAttributionLicense,whichpermitsunrestricted use,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding: This work was supported by th