FAM105A通过caspase依赖性途径和Bcl-2家族诱导细胞凋亡  

The Apoptosis Induced by FAM105A Through Bcl-2 Family and Caspase Dependent Pathway

作　　者：袁梦[1] 赵永浩[1] 王云姝[1] 刘亦倩[1] 张弦[1] 许华曦[1] 张云武[1] 

机构地区：[1]厦门大学生物医学研究院,福建省神经退行性疾病与衰老研究重点实验室,福建厦门361005

出　　处：《厦门大学学报（自然科学版）》2011年第6期1065-1069,共5页Journal of Xiamen University：Natural Science

基　　金：国家自然科学基金项目(30973150);国家重点基础研究发展计划(973)前期研究专项项目(2010CB535004);国家科技重大专项项目(2009ZX09103-731);福建省自然科学杰出青年基金项目(2009J06022)

摘　　要：在多细胞有机体中,细胞凋亡对调节正常细胞活动和发育起着关键作用.对参与细胞凋亡的蛋白的鉴定及其机制的阐明具有重要意义.FAM 105 A是新发现的促凋亡基因,过表达会导致细胞凋亡.研究了FAM105A促进细胞凋亡的潜在机制,结果表明,在HEK293T细胞中过表达FAM105A会导致caspase-3和caspase-9的剪切/激活,同时伴随着多聚ADP-核糖聚合酶(poly ADP ribose polymerase,PARP)的切割/失活.此外,过表达FAM105A能诱导细胞色素c(Cyt c)从线粒体释放到胞质,促凋亡蛋白Bax的表达水平升高,而抗凋亡蛋白Bcl-2的表达水平下降.这些结果表明FAM105A诱导的细胞凋亡过程需要caspase依赖性途径和Bcl-2家族共同参与.Apoptosis plays a crucial role in mediating normal cellular activities and development in multicellular organisms.Characterization and mechanistic elucidation of proteins involved in apoptosis are important for understanding this process.FAM105A is a newly identified pro-apoptotic gene,whose overexpression results in cell apoptosis.However,the mechanism underlying FAM105A-mediated apoptosis remains elusive.In this study,it was found that overexpression of FAM105A in HEK293T cells induced cleavage/activation of caspase-3 and caspase-9,accompanied with cleavage/inactivation of the poly ADP-ribose polymerase（PARP）.In addition,overexpression of FAM105A induced cytochrome c（Cyt c）release from mitochondria to the cytosol.Moreover,overexpression of FAM105A increased and decreased the levels of pro-apoptotic Bax and anti-apoptotic Bcl-2,respectively.These results suggest that FAM105A-mediated apoptosis requires the involvement of the caspase-dependent pathway and the Bcl-2 family.

关 键 词：FAM105A 细胞凋亡 CASPASES 细胞色素C BCL-2家族 

分 类 号：Q291[生物学—细胞生物学]