泛素蛋白酶体途径在癫痫发病机制中的作用研究进展  

Research advances on the role of ubiquitin-proteasome pathway in the pathogenesis of epilepsy

作　　者：张贺博 刘晓亮[1] 赵彦艳[1] ZHANG He-bo;LIU Xiao-liang;ZHAO Yan-yan(Department of Clinical Genetics,Shengjing Hospital of China Medical University,Liaoning Province,Shenyang 110001,China)

机构地区：[1]中国医科大学附属盛京医院临床遗传科,辽宁沈阳110001

出　　处：《中国当代医药》2020年第29期21-24,共4页China Modern Medicine

基　　金：国家重点研发计划生殖健康及重大出生缺陷防控研究重点专项(2016YFC1000702)。

摘　　要：癫痫是一种常见的慢性神经系统疾病,其特征是由大脑神经元过度放电引起的突发性和复发性发作以及暂时性中枢神经系统功能障碍。近年来研究表明,癫痫的发生与离子通道、神经递质、突触连接等有密切联系。泛素蛋白酶体途径是生物体内蛋白质降解的重要途径,其调控了细胞的许多重要生理过程。泛素化修饰的底物中有很多是影响中枢神经兴奋性的离子通道蛋白,如钠离子通道、钾离子通道等电压门控离子通道,以及AMPA受体、NMDA受体等配体门控离子通道。泛素化修饰通过调控这些通道蛋白表达水平,进一步影响神经元的兴奋性,与癫痫的发生密切相关。Epilepsy is a common chronic nervous system disease,which is characterized by sudden,recurrent seizures and temporary central nervous system dysfunction caused by excessive discharge of brain neurons.Recent studies have shown that the occurrence of epilepsy is closely related to ion channels,neurotransmitters and synaptic connections.Ubiquitin-proteasome pathway is an important protein degradation pathway in vivo,which regulates many cellular physiological processes.Many substrates modified by ubiquitination are ion channel that affect central nervous excitability,such as voltage-gated ion channels including sodium channels and potassium channels as well as ligand-gated ion channels including AMPA receptor and NMDA receptor.Ubiquitination affects neuronal excitability by regulating the expression level of these channel proteins,which is closely related to the pathogenesis of epilepsy.

关 键 词：泛素化 泛素E3连接酶 癫痫 离子通道 

分 类 号：R742[医药卫生—神经病学与精神病学]