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HERG(human ether-a-go-go-related gene)编码的钾通道介导快速激活延迟整流钾电流(IKr)。IKr在心肌动作电位复极中发挥极其关键的作用,IKr的减弱可延长心肌动作电位时程,导致长QT综合征(LQTS)。HERG突变和HERG钾通道的药物性阻滞是LQTS的常见原因之一。心脏HERG钾通道功能受众多因素的调控,该通道的磷酸化是重要的调控因素之一。现有报道证实HERG钾通道的调节由蛋白激酶(protein kinases A、C和protein tyrosine kinases Src等)介导完成。
Potassium channels encoded by HERG (human ether-a-go-go-related gene) mediate the rapid activation of delayed rectifier potassium currents (IKr). IKr plays a crucial role in repolarization of myocardial action potentials. Weakening of IKr prolongs the action potential duration of myocardium and leads to long QT syndrome (LQTS). HERG mutations and HERG potassium channel pharmacological block is one of the common causes of LQTS. Cardiac function of HERG potassium channels is regulated by many factors, and phosphorylation of this channel is one of the important regulatory factors. It has been reported that the regulation of HERG potassium channel is mediated by protein kinases A, C and protein tyrosine kinases Src.