Spontanenous apoptosis through caspase-3 activated by transfection of naofen in HEK293 cells
作者单位：Department of PharmacologyAichi Medical University School of MedicineNagakuteAichi-gunAichi-PrefectureJapan Health Reserch CenterAichi Gakuin UniversityNagoyaAichi-PrefectureJapan
会议名称：《2008北京国际生理科学学术大会》
会议日期：2008年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 10[医学]
关 键 词：naofen caspase-3 apoptosis TNF-α
摘 要：正Naofen（GenBank ID:EF613262）,a novel WD40-repeat-domain（WRD）containing protein,has recently been cloned from cDNA library of rat’s brain/spinal cord using anti-shigatoxin 2（STX2）*** containing proteins have a wide variety of functions including signal transductions,apoptosis,cell proliferation,and many are involved in coordinating protein-protein interactions in large multiprotein *** STX2 induces apoptosis in *** the present study,we evaluated the participation of naofen in apoptosis of HEK293 cells and further the roles of naofen in tumor necrosis factor alpha（TNF-α）-induced *** results showed that:（1）Naofen is ubiquitously distributed throughout the body of rat,with a maximal concentration in testis.（2） The transfection with an empty plasmid as control did not alter the caspase activities,whereas full-length naofen transfection increased them:Caspase-8 and -9 activities increased at 12 h after naofen transfection,reached maximum at 36 h and then ***-3 activities also increased from 24 h and continued till 72 h.（3）Clones of HEK293,which stably expressed naofen,also continuously elicited high caspase-3 activities.（4）Treatment with TNF-αor dexomethasone,both apoptosis inducers,significantly increased naofen mRNA expressions in a concentration -dependent manner.（5）In the clones,TNF-αincreased the caspase-3 activities to a much greater *** addition,higher susceptibility to cells was demonstrated with a flowcytometry utilizing the fluorescent labeled annexin V as a *** conclude that naofen is an important cytosolic protein,playing a principal role in cell apoptosis via promoting the caspase-3 activities,and that naofen may mediate the caspase-activation in the TNF-α-induced apoptosis.