Regulated Cell Death: Signaling and Mechanisms

被引:203
作者
Ashkenazi, Avi [1 ]
Salvesen, Guy [2 ]
机构
[1] Genentech Inc, San Francisco, CA 94080 USA
[2] Sanford Burnham Med Res Inst, La Jolla, CA 92037 USA
来源
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, VOL 30 | 2014年 / 30卷
关键词
apoptosis; necroptosis; death receptor; caspase; tumor necrosis factor; TNF; receptor interacting protein; RIP; MIXED LINEAGE KINASE; CASPASE-8; ACTIVATION; LONG FORM; MOLECULAR-MECHANISMS; PROGRAMMED NECROSIS; EXTRINSIC APOPTOSIS; MEDIATED APOPTOSIS; DOMAIN FADD; GRANZYME-B; RECEPTOR;
D O I
10.1146/annurev-cellbio-100913-013226
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cell turnover is a fundamental feature in metazoans. Cells can die passively, as a consequence of severe damage to their structural integrity, or actively, owing to a more confined biological disruption such as DNA damage. Passive cell death is uncontrolled and often harmful to the organism. In contrast, active cell death is tightly regulated and serves to support the organism's life. Apoptosis-the primary form of regulated cell death-is relatively well defined. Necroptosis-an alternative, distinct kind of regulated cell death discovered more recently-is less well understood. Apoptosis and necroptosis can be triggered either from within the cell or by extracellular stimuli. Certain signaling components, including several death ligands and receptors, can regulate both processes. Whereas apoptosis is triggered and executed via intracellular proteases called caspases, necroptosis is suppressed by caspase activity. Here we highlight current understanding of the key signaling mechanisms that control regulated cell death.
引用
收藏
页码:337 / 356
页数:20
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