Cx43缝隙连接蛋白羧基末端磷酸化修饰对其功能的调控及其在脑缺血中的研究进展  

Regulation of Cx43 gap junction protein function by carboxyl terminal phosphorylation and its research progress in cerebral ischemia

作　　者：左夏林[1] 唐艳艳 李孔平 彭林辉 徐恩[1] ZUO Xialin;TANG Yanyan;LI Kongping;PENG Linhui;XU En(Institute of Neurosciences,the Second Affiliated Hospital of Guangzhou Medical University,Guangzhou 510260,China)

机构地区：[1]广州医科大学神经科学研究所,广州医科大学附属第二医院神经内科,广州510260

出　　处：《实用医学杂志》2021年第21期2804-2808,共5页The Journal of Practical Medicine

基　　金：国家自然科学基金项目(编号:81971233);广州市科技计划项目(编号:202102010056)。

摘　　要：缝隙连接(gap junction,GJ)是由连接蛋白(connexin,Cx)构成的一种特殊的细胞膜结构。小分子物质通过GJ在相邻细胞之间进行物质和能量交换的现象称为缝隙连接细胞间通讯(gap junction intercellular communication,GJIC)。连接蛋白43(connexin 43,Cx43)是参与形成GJIC的主要连接蛋白,其羧基末端(carboxyl terminal,CT)富含的丝氨酸和脯氨酸是Cx43磷酸化修饰的潜在靶点,亦是蛋白相互作用的结构域。Cx43羧基末端的磷酸化修饰调控着Cx43的转运、GJ的组装和降解、GJ通道的门控,对于调控神经系统GJIC的功能至关重要。本文皆在综述目前对Cx43羧基末端磷酸化修饰的认识,Cx43羧基末端磷酸化修饰对GJIC的影响以及Cx43在脑缺血中的作用。Gap junction(GJ)is a special cell membrane structure composed of connexin protein(Cx).The exchange of material and energy between adjacent cells through GJ is called gap junction cell communication(GJIC). Junction protein connexin 43(Cx43)is the main junction protein involved in the formation of GJIC. The serine and proline rich in Carboxyl terminal(CT)at the end of its carboxy group are potential targets for Cx43 phosphorylation modification,and important domains of protein interaction. The phosphorylation of Cx43 carboxy terminal regulates the transport of Cx43,the assembly and degradation of GJ,and the gating of GJ channel,which is very important to regulate GJIC in neurous system. This review summarizes the current understanding of Cx43 carboxy terminal phosphorylation modification and the effect of Cx43 phosphorylation modification on GJIC,and provides feasible ideas for further research in cerebral ischemia.

关 键 词：CX43 羧基末端 磷酸化修饰 缝隙连接通讯 脑缺血 

分 类 号：R741[医药卫生—神经病学与精神病学]