中文摘要：

脯氨酸引导的丝/苏氨酸蛋白酶——细胞周期蛋白依赖性蛋白激酶5（cyclin-dependent kinase5,Cdk5）是细胞周期素依赖的蛋白酶家族中一个特殊成员。Cdk5不参与细胞周期调控,其活化需要与神经元内广泛表达的激活因子——p35或p39相结合。正常情况下,Cdk5的转录及活性受到体内相关机制的严格调控。在神经系统发育及成熟阶段,Cdk5通过磷酸化细胞骨架蛋白、信号分子以及调节蛋白等众多底物蛋白的特异性丝/苏氨酸位点,在神经元的迁移分化、存活和突触的发生、信息传递、可塑性等诸多方面发挥重要的作用。此外,在一些病理条件下,p35的病理性剪切和Cdk5/p25的形成所导致的Cdk5活性失调及其亚细胞分布改变则促进了神经元的凋亡或死亡,参与了阿尔茨海默氏病（Alzheimer＇s disease,AD）、帕金森氏病（Parkinson’s disease,PD）、亨廷顿氏病（Huntington’s disease,HD）以及脊髓侧索硬化症（amyotrophiclateralsclerosis,ALS）等众多神经退行性疾病的发生发展过程。本文综述了Cdk5在中枢神经系统发育和神经退行性疾病中的作用研究方面的进展。

英文摘要：

Cyclin-dependent kinase 5（Cdk5） is a proline-directed serine/threonine kinase,and plays multiple roles in neuron development and synaptic plasticity.The active form of Cdk5 is found primarily in the central nervous system（CNS） due to its activator proteins p35 or p39 ubiquitously expressed in neuronal cells.Normally,the transcription and activity of Cdk5 are strictly regulated by several ways.In the physiological condition,Cdk5 plays a key role in the CNS development by phosphorylating the specific serine or threonine site of numerous substrate proteins that are closely associated with the neuronal migration,synaptogenesis,synaptic transmission as well as synaptic plasticity.Under pathological conditions,p35 can be truncated into p25,which can strongly and consistently activate Cdk5,change the cellular localization of Cdk5 and lead to neuronal death ultimately.The increasing evidence has showed that Cdk5 is involved in the pathogenesis of many neurodegenerative diseases,such as Alzheimer＇s disease,Parkinson＇s disease,Huntington＇s disease and amyotrophic lateral sclerosis etc.,indicating that Cdk5 may be a potential target in the treatment of the neurodegenerative diseases.In this article,we reviewed the recent progress regarding the roles of Cdk5 in CNS development and neurodegenerative diseases.