论文部分内容阅读
缝隙连接是介导相邻细胞间直接通讯的特殊膜结构。心室肌细胞间的缝隙连接通道主要由连接蛋白43(Cx43)构成。Cx43的磷酸化状态除了快速调节通道的开放/闭合状态(单通道传导性和通道开放概率),还可通过影响Cx43的合成、转运、聚集/解聚和降解等不同环节,改变活化通道数量,最终实现对缝隙连接功能的调控。迄今,已发现多种激酶和蛋白磷酸酶可直接和(或)间接调控Cx43羧基末端的丝氨酸残基和酪氨酸残基的磷酸化状态,从而影响缝隙连接通道的功能。磷酸化/去磷酸化影响Cx43和缝隙连接通道功能的确切作用和具体机制未明。本文就Cx43磷酸化状态与心脏缝隙连接通道功能的关系作一综述。
Gap junctions are special membrane structures that mediate direct communication between adjacent cells. The gap junctional channel between ventricular myocytes mainly consists of connexin 43 (Cx43). Phosphorylation state of Cx43 can not only rapidly regulate the open / closed state of the channel (single-channel conductivity and channel open probability), but also change the number of activated channels by affecting different aspects of Cx43 synthesis, transport, aggregation / depolymerization and degradation, Finally realize the function of gap connection regulation. Hitherto, it has been discovered that various kinases and protein phosphatases directly and / or indirectly regulate the phosphorylation status of the C-terminal carboxyl-terminal serine and tyrosine residues, thereby affecting the function of the gap junctional pathway. The exact role and specific mechanisms of phosphorylation / dephosphorylation affecting the function of Cx43 and gap junctional channels are unknown. This article reviews the relationship between Cx43 phosphorylation status and cardiac gap junctional channel function.