中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2007, (3): 326-
p53转录非依赖活性介导细胞凋亡
钱呈睿,葛海良,王 颖*
上海交通大学医学院上海市免疫学研究所,上海200025
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。
关键词:p53;线粒体;转录非依赖凋亡;细胞凋亡
 
p53: pro-death factor that directly targets mitochondria for triggering apoptosis
QIAN Chengrui, GE Hailiang, WANG Ying*
Shanghai Institute of Immunology, Medical School of Shanghai Jiaotong University, Shanghai 200025, China
Abstract: 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 highlights the remarkable relationship between transcription-dependent and -independent apoptotic pathways.
Key words: p53; mitochondria; transcription-independent; apoptosis
 
首页 | 刊物简介 | 编委会 | 投稿须知 | 广告业务 | 过刊浏览 | 联系我们
中国科学院上海生命科学信息中心《生命科学》编辑部
Copyright © 2012-2015 《生命科学》编辑部 All Rights Reserved.
沪ICP备05033115号-30
您是第2954380 位访问者,欢迎!