CELLULAR-RESPONSES TO DNA-DAMAGE - CELL-CYCLE CHECKPOINTS, APOPTOSIS AND THE ROLES OF P53 AND ATM

被引：236

作者：

ENOCH, T ^{[1
]}

NORBURY, C ^{[1
]}

机构：

[1] UNIV OXFORD, JOHN RADCLIFFE HOSP,INST MOLEC MED,ICRF, MOLEC ONCOL LAB, OXFORD OX3 9DU, ENGLAND

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 1995年 / 20卷 / 10期

关键词：

D O I：

10.1016/S0968-0004(00)89093-3

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：

'Checkpoint' controls arrest the cell cycle after DNA damage, allowing repair to take place before mutations can be perpetuated. In multicellular organisms, DNA damage can also induce apoptotic cell death, protecting the organism at the expense of the individual cell. How does a cell 'choose' between cycle arrest and death? Analysis of two human tumour suppressor proteins, p53 and the ATM (ataxia-telangiectasia mutated) gene product, may provide some answers.

引用

页码：426 / 430

页数：5

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