NEMO Inhibits Programmed Necrosis in an NFκB-Independent Manner by Restraining RIP1 英文参考文献.docVIP

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NEMO Inhibits Programmed Necrosis in an NFκB-Independent Manner by Restraining RIP1 英文参考文献.doc

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NEMO Inhibits Programmed Necrosis in an NFκB-Independent Manner by Restraining RIP1 英文参考文献

NEMOInhibitsProgrammedNecrosisinanNFkB- IndependentMannerbyRestrainingRIP1 MarieAnneO’Donnell*.,HidenoriHase.¤,DianaLegarda,AdrianT.Ting* ImmunologyInstitute,MountSinaiSchoolofMedicine,NewYork,NewYork,UnitedStatesofAmerica Abstract TNFcantriggertwoopposingresponses:cellsurvivalandcelldeath.TNFR1activatescaspasesthatorchestrateapoptosis but some cell types switch to anecrotic death when treated with caspase inhibitors. Several genesthat are required to orchestratecelldeathbyprogrammednecrosishavebeenidentified,suchasthekinaseRIP1,butverylittleisknownabout theinhibitorysignalsthatkeepthisnecroticcelldeathpathwayincheck.WedemonstratethatTcellslackingtheregulatory subunitofIKK,NFkBessentialmodifier(NEMO),arehypersensitivetoprogrammednecrosiswhenstimulatedwithTNFin thepresenceofcaspaseinhibitors.Surprisingly,thispro-survivalactivityofNEMOisindependentofNFkB-mediatedgene transcription.Instead,NEMOinhibitsnecrosisbybindingtoubiquitinatedRIP1torestrainRIP1fromengagingthenecrotic deathpathway.IntheabsenceofNEMO,orifubiquitinationofRIP1isblocked,necrosisensueswhencaspasesareblocked. TheseresultsindicatethatrecruitmentofNEMOtoubiquitinatedRIP1isakeystepintheTNFR1signalingpathwaythat determineswhetherRIP1triggersanecroticdeathresponse. Citation: O’DonnellMA,HaseH, LegardaD,TingAT(2012)NEMO InhibitsProgrammed Necrosis inanNFkB-IndependentMannerbyRestrainingRIP1.PLoS ONE7(7):e41238.doi:10.1371/journal.pone.0041238 Editor:DhyanChandra,RoswellParkCancerInstitute,UnitedStatesofAmerica ReceivedDecember2,2010;AcceptedJune25,2012;PublishedJuly26,2012 Copyright: ? 2012 O’Donnell et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited. Funding:ThisworkwassupportedbyNationalInstitutesofHealthgrantsAI052417andagrantfromtheNewYorkChapteroftheArthritisFoundationtoA.T.T. M.A.O.isarecipientofaResearchFellowshipAwardfromth