Caspase 2 in apoptosis, the DNA damage response and tumour suppression: enigma no more?

被引：120

作者：

Kumar, Sharad ^{[1
]}

机构：

[1] SA Pathol, Dept Haematol, Ctr Canc Biol, Adelaide, SA 5000, Australia

来源：

NATURE REVIEWS CANCER | 2009年 / 9卷 / 12期

基金：

英国医学研究理事会;

关键词：

STRESS-INDUCED APOPTOSIS; CYTOCHROME-C RELEASE; ENDOPLASMIC-RETICULUM STRESS; ACUTE LYMPHOBLASTIC-LEUKEMIA; ETOPOSIDE-INDUCED APOPTOSIS; PROGRAMMED CELL-DEATH; CASPASE-2-INDUCED APOPTOSIS; ATAXIA-TELANGIECTASIA; NUCLEAR-LOCALIZATION; INITIATOR CASPASES;

D O I：

10.1038/nrc2745

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Aberrations in proteins that control apoptosis and cell survival are common in cancer. These aberrations often reside in signalling proteins that control the activation of the apoptotic machinery or in the Bcl-2 family of proteins that control caspase activation. Recent evidence suggests that caspase 2, one of the most evolutionarily conserved caspases, may have multiple roles in the DNA damage response, cell cycle regulation and tumour suppression. These findings are unexpected and have important implications for our understanding of tumorigenesis and the treatment of cancer.

引用

页码：897 / 903

页数：7

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