《Bcl-2家族蛋白参与调节CD3ε和5-氟尿嘧啶介导的T淋巴细胞凋亡》.pdfVIP

猩窒笠墅墨塞筮蛋自叁皇塑堇垡堕!塑』：氩星堕喧金昱的!进旦绁照遇圭筮!翅 程宏刘彦信张锦春刘士廉郑德先 (中国医学科学院基础医学研究所中国协和医科大学基础医学院 医学分子生物学国家重点实验室，北京100005) 中国图书分类号R392．12文献标识码A 文章编号1∞¨翻x(20帖)01．0017-05 [摘要】 亡的分子机制，为相关肿瘤的治疗提供依据。方法：用CD3e特异的单克隆抗体(200vcCn[11)和5．FU(2．5tc／mD单独或联合刺激 JK、TJK和，13Ⅸ细胞，诱导细胞凋亡，用MTS比色法检测细胞死亡率，用Westernblot检测Bid的表达和活化。用脂质体的方法 和5．FU诱导的T淋巴细胞凋亡的调节，Bcl-2过表达能显著抑制T淋巴细胞对5．FU的敏感性。 [关键词】CD3e；5．FU；Bid；Bcl．2；细胞凋亡 Bcl-2 T mediated 5-FU familyproteinsregulatelymphocyteapoptosis by锄￡and De-Xian．National Molec— Yan-Xin，ZHANGJin-Chun，LIUShi-Lian，ZHENG LaboratoryofMedical CHENG胁昭，LIU ular BasicMedical Medical UnionMedical Sciences，ChineseAcademyof SciencesPeking Biology，Instituteof College， 100005，China B,彬ng the ofBel-2 onT mediatedCD3eand／or [Abstract]Objective：Toinvestigateregulationfamily lymphocyteapoptosis by 5一Fu(5一nu— to anovel ofthe andthe fortheclinic of leukemia． omumcil)and therapy provide insight apoptosissi朗alillgpathwayimplication T-lymphocyte cells with and／or 34h．MTS was and-13JKstimulatedanti—CD8mAb(200 Methods：JK，TJK tcCml)cmss-link5-FU(2．5倒1111)forassay usedtodetectcell andBidactivationand weredetctedWesternblot．Bcl-2 was trails— viability．Bel-2 expression by expressionplasmidstably fectedinto cells wasactivatedintheTJK induced TJK method(250心，300Volts)．Remits：Bid apoptosis byCD3￡specific byelectroporation inthe cotreatedwiththe moll- monoclonalor5一FU．The rateandBi