Aguda B D
Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ontario, Canada.
Oncogene. 1999 May 6;18(18):2846-51. doi: 10.1038/sj.onc.1202462.
The G2-M checkpoint in the cell cycle is identified with a set of phosphorylation-dephosphorylation (PD) cycles involving Cdc25 and the maturation-promoting factor (MPF); these PD cycles are coupled in a way that generates an instability. This instability arises out of a transcritical bifurcation which could be exploited by the G2 DNA damage checkpoint pathway in order to arrest or delay entry into mitosis. The coupling between PD cycles involving Wee1 and MPF does not lead to an instability and therefore Wee1 may not be a crucial target of the checkpoint pathway. A set of PD cycles exhibiting transcritical bifurcation also possesses the integrative ability of a checkpoint for 'checking' that prerequisites are satisfied prior to the next cell cycle event. Such a set of coupled PD cycles is suggested to be a core mechanism of cell cycle checkpoints.
细胞周期中的G2-M检查点与一组涉及Cdc25和成熟促进因子（MPF）的磷酸化-去磷酸化（PD）循环相关；这些PD循环以一种产生不稳定性的方式相互耦合。这种不稳定性源于一个跨临界分岔，G2 DNA损伤检查点通路可以利用这一分岔来阻止或延迟进入有丝分裂。涉及Wee1和MPF的PD循环之间的耦合不会导致不稳定性，因此Wee1可能不是检查点通路的关键靶点。一组表现出跨临界分岔的PD循环还具有检查点的整合能力，可“检查”在下一个细胞周期事件之前先决条件是否得到满足。这样一组耦合的PD循环被认为是细胞周期检查点的核心机制。
