Stress-induced apoptosis and the sphingomyelin pathway

被引:213
作者
Pena, LA
Fuks, Z
Kolesnick, R
机构
[1] MEM SLOAN KETTERING CANC CTR,LAB SIGNAL TRANSDUCT,NEW YORK,NY 10021
[2] MEM SLOAN KETTERING CANC CTR,DEPT RADIAT ONCOL,NEW YORK,NY 10021
关键词
apoptosis; sphingomyelin; sphingomyelinase; ceramide; ICE proteases; environmental stress; cytokines;
D O I
10.1016/S0006-2952(96)00834-9
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The sphingomyelin pathway is a ubiquitous, evolutionarily conserved signaling system initiated by hydrolysis of the plasma membrane phospholipid sphingomyelin to generate the second messenger ceramide. Sphingomyelin degradation is catalyzed by acid and neutral sphingomyelinase (SMase) isoforms. Most, if not ail mammalian cells, appear capable of signaling though the sphingomyelin pathway. Diverse receptor types and environmental stresses utilize the sphingomyelin pathway as a downstream effector system. In some cellular systems, ceramide initiates differentiation or cell proliferation, while in other systems, ceramide signals apoptosis. Recent investigations link the activation of neutral SMase to the extracellular signal regulated kinase (ERK) cascade and pro-inflammatory responses, and acid SMase to the stress-activated protein kinase/c-jun kinase (SAPK/JNK) cascade and apoptotic responses. Environmental stresses act directly on membrane to activate acid pH-dependent sphingomyelinase (ASMase), whereas cytokine receptors signal ASMase activation through motifs termed death domains. The present review focuses on mechanisms of activation of ASMase and on ceramide signaling of the apoptotic response. (C) 1997 Elsevier Science Inc.
引用
收藏
页码:615 / 621
页数:7
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