去泛素化酶USP48调节TNFα信号转导通路中TRAF2蛋白稳定性的研究的开题报告-第一文库 | 海量文档资源下载与分享平台

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去泛素化酶USP48调节TNFα信号转导通路中TRAF2蛋白稳定性的研究的开题报告Title:InvestigationofhowdeubiquitinaseUSP48regulatesthestabilityofTRAF2proteininTNFαsignalingpathwayBackgroundandsignificance:TNFαisanimportantcytokineinimmuneresponseandinflammation.Itcanactivatevarioussignalingpathways,includingNF-κBandMAPK,toregulategeneexpressionandcellfunctions.OneofthekeycomponentsinTNFαsignalingistumornecrosisfactorreceptor-associatedfactor2(TRAF2),whichcaninteractwithTNFreceptorandactivatedownstreamsignaltransductioncascades.However,TRAF2proteinisunstableandsubjecttodegradationbyproteasomes.Therefore,understandingthemechanismsthatcontrolTRAF2stabilityiscriticalforcontrollingTNFαsignaling.Ubiquitinationisapost-translationalmodificationthatregulatesproteindegradationandtrafficking.Ubiquitinligases(E3s)canattachubiquitinmoleculestolysineresiduesoftargetproteins,leadingtotheirproteasomaldegradationorsortingintodifferentcellularcompartments.Conversely,deubiquitinases(DUBs)canremoveubiquitinchainsfromtargetproteinsandaltertheirfate.USP48isaDUBthathasbeenimplicatedintheregulationofvariouscellularprocesses,includingDNAdamageresponse,cellcycleprogression,andautophagy.RecentstudieshavesuggestedthatUSP48alsoplaysaroleinTNFαsignalingbystabilizingTRAF2protein.However,themolecularmechanismofhowUSP48regulatesTRAF2stabilityandTNFαsignalingremainsunclear.Researchaims:ThemainobjectiveofthisresearchistoinvestigatetheroleofUSP48inregulatingTRAF2proteinstabilityinTNFαsignalingpathwayandtoelucidatetheunderlyingmolecularmechanisms.Specifically,weaimto:1.ConfirmtheinteractionbetweenUSP48andTRAF2inTNFα-stimulatedcellsusingco-immunoprecipitationassays2.DeterminetheeffectofUSP48onTRAF2proteinstabilityusingproteinturnoverassaysandimmunoblotting3.InvestigatetheinfluenceofUSP48onTNFαsignalingpathwaybymeasuringNF-κBandMAPKpathwayactivityusingluciferasereporterassays4.ExplorethepotentialubiquitinationsitesandE3ligasesthattargetTRAF2fordegradationandassesshowUSP48counteractsthisprocessMethodology:Thefollowingmethodologie