O'Connell M J, Walworth N C, Carr A M
Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, Locked Bag 1, A'Beckett Street, Melbourne, Victoria 8006, Australia.
Trends Cell Biol. 2000 Jul;10(7):296-303. doi: 10.1016/s0962-8924(00)01773-6.
DNA damage causes cell-cycle delay before S phase, during replication and before mitosis. This involves a number of highly conserved proteins that sense DNA damage and signal the cell-cycle machinery. Kinases that were initially discovered in yeast model systems have recently been shown to regulate the regulators of cyclin-dependent kinases and to control the stability of p53. This shows the importance of checkpoint proteins for maintaining genome stability. Here, we discuss recent data from yeast and metazoans that suggest a remarkable conservation of the organization of the G2 DNA-damage checkpoint pathway.
DNA损伤会导致细胞在S期之前、复制过程中以及有丝分裂之前出现细胞周期延迟。这涉及到许多高度保守的蛋白质，它们能够感知DNA损伤并向细胞周期机制发出信号。最初在酵母模型系统中发现的激酶最近被证明可以调节细胞周期蛋白依赖性激酶的调节因子，并控制p53的稳定性。这表明检查点蛋白对于维持基因组稳定性的重要性。在这里，我们讨论来自酵母和后生动物的最新数据，这些数据表明G2期DNA损伤检查点途径的组织具有显著的保守性。
