Functional Identification of Api5 as a Suppressor of E2F-Dependent Apoptosis In Vivo 英文参考文献.docVIP

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Functional Identification of Api5 as a Suppressor of E2F-Dependent Apoptosis In Vivo 英文参考文献.doc

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Functional Identification of Api5 as a Suppressor of E2F-Dependent Apoptosis In Vivo 英文参考文献

FunctionalIdentificationofApi5 asaSuppressorofE2F-Dependent ApoptosisInVivo Erick J.Morris1,2,William A.Michaud1,2,3,4,Jun-Yuan Ji1,2,Nam-Sung Moon1,2,James W. Rocco1,2,3,4 Nicholas J.Dyson1,2* , 1 Massachusetts General Hospital Cancer Center, Laboratory of Molecular Oncology, Charlestown, Massachusetts, United States of America, 2 Harvard Medical School, Boston, Massachusetts, United States of America, 3 Division of Surgical Oncology, Massachusetts General Hospital, Boston, Massachusetts, United States of America, 4 MassachusettsEyeandEarInfirmary,Boston,Massachusetts,UnitedStatesofAmerica RetinoblastomaproteinandE2-promoterbindingfactor(E2F)familymembersareimportantregulatorsofG1-Sphase progression.DeregulatedE2Falsosensitizescellstoapoptosis,butthisaspectofE2Ffunctionispoorlyunderstood. StudiesofE2F-inducedapoptosishavemostlybeencarriedoutintissueculturecells,andtheanalysisofthefactors thatareimportantforthisprocesshasbeenrestrictedtothetestingofafewcandidategenes.UsingDrosophilaasa modelsystem,wehavegeneratedtoolsthatallowgeneticmodifiersofE2F-dependentapoptosistobeidentifiedin vivo and developed assays that allow effects on E2F-induced apoptosis to be studied in cultured cells. Genetic interactionsshowthatdE2F1-dependentapoptosisinvivoinvolvesdArk/Apaf1apoptosome-dependentactivationof bothinitiatorandeffectorcaspasesandissensitivetolevelsofDrosophilainhibitorofapoptosis-1(dIAP1).Usingthese approaches,wereportthesurprisingfindingthatapoptosisinhibitor-5/antiapoptosisclone-11(Api5/Aac11)isacritical determinantofdE2F1-inducedapoptosisinvivoandinvitro.Thisfunctionalinteractionoccursinmultipletissues,is specifictoE2F-inducedapoptosis,andisconservedfromfliestohumans.Interestingly,Api5/Aac11actsdownstreamof E2F and suppresses E2F-dependent apoptosis without generally blocking E2F-dependent transcription. Api5/Aac11 expressionisoftenupregulatedintumorcells,particularlyinmetastaticcells.WefindthatdepletionofApi5istumor celllethal.Thestronggeneticinteractionbetween