Malumbres Marcos, Barbacid Mariano
Cell Division and Cancer, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), 28029 Madrid, Spain.
Curr Opin Genet Dev. 2007 Feb;17(1):60-5. doi: 10.1016/j.gde.2006.12.008.
Cell division in mammalian cells is driven by protein kinases that regulate progression through the various phases of the cell cycle. Cyclin-dependent kinases (Cdks) regulate cell cycle commitment, DNA synthesis and the onset of mitosis. Kinases of the Aurora, Polo and Nek families participate in the centrosome cycle and modulate spindle function. Additional kinases such as Bub1, BubR1 and Mps1 regulate the spindle assembly checkpoint. It has been well established that misregulation of Cdks is one of the most frequent alterations in human cancer. Recent evidence indicates that mutations involving mitotic kinases are also linked to tumor development. These findings suggest novel strategies to use cell cycle kinases as targets for therapeutic intervention.
哺乳动物细胞中的细胞分裂由蛋白激酶驱动,这些蛋白激酶调节细胞周期各阶段的进程。细胞周期蛋白依赖性激酶(Cdks)调节细胞周期的启动、DNA合成以及有丝分裂的开始。极光激酶、Polo激酶和Nek激酶家族参与中心体周期并调节纺锤体功能。其他激酶,如Bub1、BubR1和Mps1,调节纺锤体组装检查点。众所周知,Cdks的失调是人类癌症中最常见的改变之一。最近的证据表明,涉及有丝分裂激酶的突变也与肿瘤发展有关。这些发现提示了将细胞周期激酶作为治疗干预靶点的新策略。