27891.b23通過抑制eg5atp酶活性抑制eg5對微管的解聚

1、中國科學技術大學碩士學位論文B23通過抑制Eg5ATP酶活性抑制Eg5對微管的解聚姓名：汪國興申請學位級別：碩士專業(yè)：細胞生物學指導教師：吳緬20100501AbstractABSTRACTNucleophosmin／B23，allabundantnucleolarprotein，playsmultiplerolesineeUgrowthandproliferationTherearetwoB23isoformsSubtype1，whi

2、chisthefulllengthofB23，is35aminoacidslongerthanSubtype2C—terminusofB23，whichiscalledDNAandRNABindingDomain(DRBD)，iStendtomutanted，anditsmutationscouldinduceAcute‘“myeloidleukemia(AML)ItisreportedthatB23mutationsleadtoabe

3、rrantlocalizationoftheB23proteinintothecytoplasmandpromoteAMLoccurrenceDespiteitsfunctionsinsidethenucleusiswell—studied，functionsofB23inthecytoplasmremainselusiveTherefore，itisunclearexactlythathowB23mutationsleadtoAMLW

4、ethentriedtofindthemeaningofB23locatesinthecytos01FirstlyaYeastTwohybridsystemWasusedtoscreenB23novelinteractpartnersAndamemberofthekinesinfamilyE95，wasfoundandidentifiedtointeractwithB23ItisfurtherprovedthatB23directlyi

5、nteractswithE95inthecytos01ThisevidencesgivesomeindicationsaboutthefunctionofB23incytoplasmAninterestingresultwasthenfoundthatinoppositetoE95，B23promotesmicrotubule(MT)polymerizationThisWasthefirstevidencethatB23playsani

6、mportantroleinregulatingMTdynamicsincytoplasmFurtherresultsshowedthatB23regulatesMTdynamicsbydirectlyinhibitingE95ATPaseactivityItmakessensesforstudyingnovelB23functionsFurthermore，asE95isanimportantanti—neoplasmicdrugta

7、rget，andwildtypeB23couldinhibitAMLdevelopment，whethertheinhibitorsofE95suchasmimicsofDRBDofB23couldbeusedintreatingAMLpatientsisofclinicalinterestInaword，ourworkssuggestthatB23hasanimportantfunctionincytoplasmKeywords：B2