Smith Patrice D, O'Hare Michael J, Park David S
Ottawa Health Research Institute, Neuroscience Group, University of Ottawa, Ottawa, Ontario, Canada.
Cell Cycle. 2004 Mar;3(3):289-91. Epub 2004 Mar 1.
While the requirement of CDKs in cell cycle control is well established, the participation of CDK family members in other important biological processes are now beginning to be uncovered. Paramount in these newly defined roles is the surprising involvement of CDKs in neuronal development and death. These discoveries are somewhat of a paradox considering the terminally differentiated state of neurons. This brief perspective will focus on the role of CDKs in neuronal death and neurodegeneration. In this regard, we will primarily explore two (of potentially many) ways by which CDKs may enable neuronal death. The first involves the effects of ectopic activation of cell cycle related CDKs in a terminal post mitotic environment. The second explores how cdk5, a neuron specific cdk required for normal neuronal function, can be usurped to signal death.
虽然细胞周期蛋白依赖性激酶(CDKs)在细胞周期调控中的作用已得到充分证实,但CDK家族成员在其他重要生物学过程中的参与现在才刚刚开始被揭示。在这些新定义的作用中,最重要的是CDKs令人惊讶地参与了神经元的发育和死亡。考虑到神经元的终末分化状态,这些发现多少有些自相矛盾。这篇简短的观点文章将聚焦于CDKs在神经元死亡和神经退行性变中的作用。在这方面,我们将主要探讨(可能有很多种方式中的)两种CDKs可能导致神经元死亡的途径。第一种涉及在有丝分裂后终末环境中细胞周期相关CDKs的异位激活效应。第二种探讨正常神经元功能所需的神经元特异性CDK——cdk5如何被篡夺来发出死亡信号。