HERG（human ether-a go-go-related gene）通道在心脏中高表达，编码心肌动作电位3期快速复极化电流（IKr）。HERG通道被抑制可诱发长QT综合症(LQTs)，甚至引起致命性心律失常和心源性猝死。三氧化二砷（ATO）在临床应用中最常见的不良反应是LQTs，前期研究中发现，应用临床相关浓度的ATO触发心肌细胞中SUMO化修饰。以往的研究表明蛋白质翻译后修饰影响HERG通道功能，本课题针对预测到的HERG蛋白SUMO化修饰位点，拟突变HERG蛋白的SUMO化修饰位点，构建SUMO修饰位点突变体；利用分子生物学实验和膜片钳技术，首次揭示SUMO化修饰对HERG通道的调控作用，确定HERG通道的SUMO化修饰位点及其功能；为全方位理解HERG通道的调控机制提供全新的理论依据，对有效防治药源性LQTs和心源性猝死具有重要意义。

HERG (human ether-a go-go-related gene) channel is highly expressed in the heart, encoding the IKr potassium channel for the rapid repolarization of the cardiac action potential. HERG channel block induces long QT syndrome (LQTs), and futher causes fatal arrhythmia and sudden cardiac death. The most common adverse effects of arsenic trioxide (ATO) in clinical treatment are LQTs. We have previously demonstrated use of ATO at clinically relevant concentrations triggers SUMOylation in cardiomyocytes. The previous studies have demonstrated that post-translational modification of HERG channel effects its function. In this study, we predicte the SUMOylation sites of HERG protein for the first time and constructed the different SUMO mutants. The role of SUMOylation sites of HERG protein is determined by molecular biology techniques and whole-cell patch clamp. This study may provide theoretical basis for comprehensively understanding the regulatory mechanism of HERG channel, which is of great significance for the effective prevention and treatment of drug-induced LQTs and sudden cardiac death.