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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.

DOI:10.1042/bj3220019
PMID:9078237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1218152/
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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本文引用的文献

1
The Ced-3/interleukin 1beta converting enzyme-like homolog Mch6 and the lamin-cleaving enzyme Mch2alpha are substrates for the apoptotic mediator CPP32.凋亡相关蛋白CED-3/白细胞介素1β转化酶样同源物Mch6和核纤层蛋白切割酶Mch2α是凋亡介质CPP32的底物。
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DNA-damaging agents induce both p53-dependent and p53-independent apoptosis in immature thymocytes.DNA损伤剂可诱导未成熟胸腺细胞发生p53依赖性和p53非依赖性凋亡。
Mol Pharmacol. 1996 Oct;50(4):900-11.
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In vitro activation of CPP32 and Mch3 by Mch4, a novel human apoptotic cysteine protease containing two FADD-like domains.一种含有两个FADD样结构域的新型人类凋亡半胱氨酸蛋白酶Mch4对CPP32和Mch3的体外激活作用。
Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7464-9. doi: 10.1073/pnas.93.15.7464.
4
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Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8395-400. doi: 10.1073/pnas.93.16.8395.
5
Sequential activation of three distinct ICE-like activities in Fas-ligated Jurkat cells.Fas 连接的 Jurkat 细胞中三种不同的类 ICE 活性的顺序激活。
FEBS Lett. 1996 Jul 29;390(3):299-303. doi: 10.1016/0014-5793(96)00678-3.
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