An Essential Role of the Cytoplasmic Tail of CXCR4 in G-Protein Signaling and Organogenesis 英文参考文献.docVIP
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An Essential Role of the Cytoplasmic Tail of CXCR4 in G-Protein Signaling and Organogenesis 英文参考文献
AnEssentialRoleoftheCytoplasmicTailofCXCR4inG-
ProteinSignalingandOrganogenesis
DarranG.Cronshaw,YuchunNie¤a,JanelleWaite¤b,Yong-RuiZou*
CenterforAutoimmuneandMusculoskeletalDiseases,FeinsteinInstituteforMedicalResearch,Manhasset,NewYork,UnitedStatesofAmerica
Abstract
CXCR4regulatescellproliferation,enhancescellsurvivalandinduceschemotaxis,yetmolecularmechanismsunderlyingits
signaling remain elusive. Like all other G-protein coupled receptors (GPCRs), CXCR4 delivers signals through G-protein-
dependentand-independentpathways,thelatterinvolvingitsserine-richcytoplasmictail.Toevaluatethesignalingand
biologicalcontributionofthisG-protein-independentpathway,wegeneratedmutantmicethatexpresscytoplasmictail-
truncatedCXCR4(DT)byageneknock-inapproach.WefoundthatDTmiceexhibitedmultipledevelopmentaldefects,with
notonlyG-protein-independentbutalsoG-protein-dependentsignalingeventscompletelyabolished,despiteDT’sability
tostillassociatewithG-proteins.TheseresultsrevealanessentialpositiveregulatoryroleofthecytoplasmictailinCXCR4
signaling and suggest the tail is crucial for mediating G-protein activation and initiating crosstalk between G-protein-
dependentandG-protein-independentpathwaysforcorrectGPCRsignaling.
Citation: Cronshaw DG, Nie Y, Waite J, Zou Y-R (2010) An Essential Role of the Cytoplasmic Tail of CXCR4 in G-Protein Signaling and Organogenesis. PLoS
ONE5(11):e15397.doi:10.1371/journal.pone.0015397
Editor:DeryaUnutmaz,NewYorkUniversity,UnitedStatesofAmerica
ReceivedAugust10,2010;AcceptedSeptember6,2010;PublishedNovember19,2010
Copyright: ? 2010 Cronshaw 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:ThisworkwassupportedinpartbytheDANAFoundation(CU,theSandlerProgramforAsthmaResearch(SPAR04-0179),andtheIrene
DiamondFund(SHRI1703)toY.-R.Z.Thefundershadnoroleinstudydesign,dat
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