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野生型p53诱导的细胞凋亡中CPP32和Mch3α的激活。

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

作者信息

Chandler J M, Alnemri E S, Cohen G M, MacFarlane M

机构信息

Medical Research Council Toxicology Unit, University of Leicester, U.K.

出版信息

Biochem J. 1997 Feb 15;322 ( Pt 1)(Pt 1):19-23. doi: 10.1042/bj3220019.

Abstract

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 B1. These results demonstrate a critical role for the activation of interleukin-1 beta-converting enzyme-like proteases in p53-induced apoptosis.

摘要

DNA损伤剂主要通过p53依赖途径诱导细胞凋亡。利用含有温度敏感型p53的LTR6细胞进一步剖析p53诱导细胞凋亡的机制。细胞凋亡伴随着CPP32和Mch3α的加工与激活,以及聚(ADP-核糖)聚合酶和核纤层蛋白B1的裂解。这些结果证明白细胞介素-1β转化酶样蛋白酶的激活在p53诱导的细胞凋亡中起关键作用。

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