Murray Andrew W
Department of Molecular and Cellular Biology, Biological Laboratories, Harvard University, Cambridge, MA 02138, USA.
Cell. 2004 Jan 23;116(2):221-34. doi: 10.1016/s0092-8674(03)01080-8.
I discuss advances in the cell cycle in the 21 years since cyclin was discovered. The surprising redundancy amongst the classical cyclins (A, B, and E) and cyclin-dependent kinases (Cdk1 and Cdk2) show that the important differences between these proteins are when and where they are expressed rather than the proteins they phosphorylate. Although the broad principles of the cell cycle oscillator are widely accepted, we are surprisingly ignorant of its detailed mechanism. This is especially true of the anaphase promoting complex (APC), the machine that triggers chromosome segregation and the exit of mitosis by targeting securin and mitotic cyclins for destruction. I discuss how a cyclin/Cdk-based engine could have evolved to assume control of the cell cycle from other, older protein kinases.
我讨论了自细胞周期蛋白被发现以来21年间细胞周期的进展。经典细胞周期蛋白(A、B和E)与细胞周期蛋白依赖性激酶(Cdk1和Cdk2)之间惊人的冗余表明,这些蛋白质之间的重要差异在于它们表达的时间和位置,而非它们所磷酸化的蛋白质。尽管细胞周期振荡器的广泛原理已被广泛接受,但令人惊讶的是,我们对其详细机制却知之甚少。后期促进复合体(APC)尤其如此,该复合体通过靶向切割蛋白和有丝分裂细胞周期蛋白进行降解,从而触发染色体分离和有丝分裂的退出。我讨论了基于细胞周期蛋白/细胞周期蛋白依赖性激酶的引擎是如何从其他更古老的蛋白激酶进化而来并承担起对细胞周期的控制的。