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1、ActaPhysiologicaSinica,August25,2005,57(4):433-438433http://www.actaps.com.cnResearchPaperExpressionofman,aforminhomologydomain-containinggeneinthemouselimbCUIYan-Zhen1,*,PENGYi-Feng2,TIANQi31DepartmentofEnvironmentalandBiomolecularSystems,OGISchoolofScienceandEngineering,OregonHealthand
2、ScienceUniversity,20000NWWalkerRd.,Beaverton,OR97006,USA;2InstituteofReproductiveMedicine,YijishanHospital,WannanMedicalCollege,Wuhu241001,China;3DepartmentofPathology,L113,SchoolofMedicine,OregonHealthandScienceUniversity,3181SWSamJacksonParkRoad,Portland,OR97239,USAAbstract:Formindefin
3、esafamilyofstructurallyrelatedproteinsthathavetwoforminhomologydomains(FH1andFH2).Variousmutationsintheforminlocusresultinlimbdeformity,suggestingthatthesegenesplayindispensablerolesinthelimbdevelopment.HerewereporttheisolationofanovelcDNA,man,fromthemouselimb,whichcontainstwoconservedFH
4、1andFH2domains.Itsexpressionisdescribedandpossiblefunctionalsignificanceisdiscussed.Keywords:man;formin;FH1;FH2;mouselimb;cytokinesis;expressioncloning基因“慢”的克隆及其在小鼠組織中的表達(dá)崔衍貞1,*，彭弋峰2，田啟31俄勒岡醫(yī)科大學(xué)環(huán)境與生命科學(xué)系，俄勒岡州97006，美國(guó)；2皖南醫(yī)學(xué)院弋磯山醫(yī)院生殖醫(yī)學(xué)研究所，蕪湖241001；3美國(guó)俄勒岡醫(yī)科大學(xué)病理學(xué)系，俄勒岡州97239，美國(guó)摘要：Formin蛋白家族由結(jié)構(gòu)相關(guān)
5、的蛋白組成，它們都有兩個(gè)formin同源功能區(qū)(forminhomologydomains)，F(xiàn)H1和FH2。這些基因上的多種變異均導(dǎo)致動(dòng)物四肢畸形，提示這些基因在肢體發(fā)育中起重要作用。我們自小鼠肢體基因庫(kù)中分離出了一個(gè)新基因：“慢”，該基因含有FH1和FH2。我們檢測(cè)了該基因在小鼠胚胎及成體的表達(dá)情況，并對(duì)可能的功能意義進(jìn)行了討論。關(guān)鍵詞：man基因；formin蛋白；formin同源功能區(qū)：FH1和FH2；鼠四肢；細(xì)胞分裂；表達(dá)克隆中圖分類號(hào)：Q956Thefirsttwoallelesofthemouselimbdeformity(ld)mains(FH1andF
6、H2),althoughsomemembersinthismutation,whichwereisolatedinthe1960s,areamongfamilycontainathirdhomologydomainFH3[5].thoseclassicalmousemutationsthatdisruptlimbmorpho-Forminrelatedproteinsaregenerallythoughttoplaycru-genesis[1].Forminwasproposedtobetherelevantgenecialrolesincytoskeletalproc
7、esses,especiallyincytokine-becauseinthreeofthefiveldallelestheC-terminaldo-sisandestablishmentofcellpolarity[6].Consistentwiththis,mainwasdisrupted[2].Overthelasttenyears,afamilyofinteractionsoftheseproteinswithactincablesandtheirformin-relatedgeneshavebeenisolated,includ
