p53转录非依赖活性介导细胞凋亡  

p53:pro-death factor that directly targets mitochondria fortriggering apoptosis

作　　者：钱呈睿[1] 葛海良[1] 王颖[1] 

机构地区：[1]上海交通大学医学院上海市免疫学研究所,上海200025

出　　处：《生命科学》2007年第3期326-329,共4页Chinese Bulletin of Life Sciences

基　　金：国家自然科学基金项目(30572117)

摘　　要：p53主要通过两条途径诱导细胞凋亡:p53作为转录因子,促进细胞凋亡的靶基因的表达上调,如PUMA、NOXA、PIDD、p53AIP1、COP1等,并通过这些蛋白参与内源和外源凋亡途径;另一方面,胞浆中的p53能转位到线粒体,激活内源性的线粒体途径,促进凋亡。后者已成为研究p53促凋亡机制的热点。本文就p53对转录非依赖活性诱导细胞凋亡途径的研究进展作一概述。p53 exerts its tumor-suppressing activity through complicated apoptotic mechanisms. Besides as a transcriptional factor for induction of multiple apoptotic-associated gene expression, p53 also triggers apoptosis through transcription-independent pathways. Cytosol p53 protein targets mitochondrial membrane through interaction with anti- or pro-apoptotic Bcl2 family members and induces the permeabilization of mitochondrial membrane, which in turn initiates intrinsic mitochondria-mediated apoptotic pathway. This review focuses on the mechanisms of its unexpected transcription-independent pro-death programs at mitochondria and high- lights the remarkable relationship between transcription-dependent and -independent apoptotic pathways.

关 键 词：P53 线粒体 转录非依赖凋亡 细胞凋亡 

分 类 号：Q244[生物学—细胞生物学] Q255