Activation of CPP32 and Mch3 alpha in wild-type p53-induced apoptosis

被引：23
作者：
Chandler, JM
Alnemri, ES
Cohen, GM
MacFarlane, M
机构：
[1] UNIV LEICESTER, MRC, TOXICOL UNIT, LEICESTER LE1 9HN, LEICS, ENGLAND
[2] THOMAS JEFFERSON UNIV, JEFFERSON MED COLL, CTR APOPTOSIS RES, PHILADELPHIA, PA 19107 USA
[3] THOMAS JEFFERSON UNIV, JEFFERSON MED COLL, KIMMEL CANC INST, PHILADELPHIA, PA 19107 USA
来源：
BIOCHEMICAL JOURNAL | 1997年 / 322卷
关键词：
D O I：
10.1042/bj3220019
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：
DNA-damaging agents induce apoptosis primarily by a p53-dependent pathway. LTR6 cells containing a temperature-sensitive p53 were used to dissect further the mechanisms of p53-induced apoptosis. Apoptosis was accompanied by the processing and activation of CPP32 and Mch3 alpha, together with the cleavage of poly(ADP-ribose) polymerase and lamin B-1. These results demonstrate a critical role for the activation of interleukin-1 beta-converting enzyme-like proteases in p53-induced apoptosis.
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页码：19 / 23
页数：5
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