Enoch T, Norbury C
Harvard Medical School, Department of Genetics, Boston, MA 02115, USA.
Trends Biochem Sci. 1995 Oct;20(10):426-30. doi: 10.1016/s0968-0004(00)89093-3.
'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.
“关卡”控制机制在DNA损伤后使细胞周期停滞,从而在突变永久化之前进行修复。在多细胞生物中,DNA损伤还可诱导凋亡性细胞死亡,以单个细胞为代价来保护生物体。细胞如何在周期停滞和死亡之间“做出选择”?对两种人类肿瘤抑制蛋白p53和ATM(共济失调毛细血管扩张症突变)基因产物的分析或许能提供一些答案。