Division of Life Science, Molecular Neuroscience Center and State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
Trends Cell Biol. 2012 Mar;22(3):169-75. doi: 10.1016/j.tcb.2011.11.003. Epub 2011 Dec 20.
Since the identification of cyclin-dependent kinase-5 (Cdk5) as a tau kinase and member of the Cdk family almost 20 years ago, deregulation of Cdk5 activity has been linked to an array of neurodegenerative diseases. As knowledge on the etiopathological mechanisms of these diseases evolved through the years, Cdk5 has also been implicated in additional cellular events that are affected under these pathological conditions. From the role of Cdk5 in the regulation of synaptic functions to its involvement in autophagy deregulation, significant insights have been obtained regarding the role of Cdk5 as a key regulator of neurodegeneration. Here, we summarize recent findings on the involvement of Cdk5 in the pathophysiological mechanisms underlying various neurodegenerative diseases.
自 20 年前发现周期蛋白依赖性激酶-5（Cdk5）作为一种 tau 激酶和细胞周期蛋白依赖性激酶家族的成员以来，Cdk5 活性的失调与一系列神经退行性疾病有关。随着这些疾病的病因发病机制的知识多年来的发展，Cdk5 也与在这些病理条件下受影响的其他细胞事件有关。从 Cdk5 在调节突触功能中的作用到其参与自噬失调，人们对 Cdk5 作为神经退行性变的关键调节剂的作用有了重要的认识。在这里，我们总结了最近关于 Cdk5 参与各种神经退行性疾病的病理生理机制的发现。
