The enigma of caspase-2: the laymen's view

被引：100

作者：

Krumschnabel, G. ^{[1
]}

Sohm, B. ^{[1
]}

Bock, F. ^{[1
]}

Manzl, C. ^{[1
]}

Villunger, A. ^{[1
]}

机构：

[1] Innsbruck Med Univ, Div Dev Immunol, Bioctr, A-6020 Innsbruck, Austria

来源：

CELL DEATH AND DIFFERENTIATION | 2009年 / 16卷 / 02期

基金：

奥地利科学基金会; 欧盟第七框架计划;

关键词：

caspase-2; caspase activity; caspase activation platform; DNA damage; ER stress; PIDD; RAIDD; STRESS-INDUCED APOPTOSIS; CYTOCHROME-C RELEASE; PROTEIN-KINASE-C; NF-KAPPA-B; ENDOPLASMIC-RETICULUM STRESS; ETOPOSIDE-INDUCED APOPTOSIS; PROGRAMMED CELL-DEATH; MESSENGER-RNA; NUCLEAR-LOCALIZATION; MEDIATED APOPTOSIS;

D O I：

10.1038/cdd.2008.170

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Proteolysis of cellular substrates by caspases (cysteine-dependent aspartate-specific proteases) is one of the hallmarks of apoptotic cell death. Although the activation of apoptotic caspases is considered a 'late-stage' event in apoptosis signaling, past the commitment stage, one caspase family member, caspase-2, splits the cell death community into half - those searching for evidence of an apical initiator function of this molecule and those considering it as an amplifier of the apoptotic caspase cascade, at best, if relevant for apoptosis at all. This review screens past and present biochemical as well as genetic evidence for caspase-2 function in cell death signaling and beyond.

引用

页码：195 / 207

页数：13

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