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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Gating currents associated with intramembrane charge displacement in HERG potassium channels.
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Gating currents associated with intramembrane charge displacement in HERG potassium channels.

机译：与HERG钾通道中膜内电荷置换相关的门控电流。

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摘要

HERG (human ether-a-go-go-related gene) encodes a delayed rectifier K+ channel vital to normal repolarization of cardiac action potentials. Attenuation of repolarizing K+ current caused by mutations in HERG or channel block by common medications prolongs ventricular action potentials and increases the risk of arrhythmia and sudden death. The critical role of HERG in maintenance of normal cardiac electrical activity derives from its unusual gating properties. Opposite to other voltage-gated K+ channels, the rate of HERG channel inactivation is faster than activation and appears to be intrinsically voltage dependent. To investigate voltage sensor movement associated with slow activation and fast inactivation, we characterized HERG gating currents. When the cut-open oocyte voltage clamp technique was used, membrane depolarization elicited gating current with fast and slow components that differed 100-fold in their kinetics. Unlike previously studied voltage-gated K+ channels, the bulk of charge movement in HERG was protracted, consistent with the slow rate of ionic current activation. Despite similar kinetic features, fast inactivation was not derived from the fast gating component. Analysis of an inactivation-deficient mutant HERG channel and a Markov kinetic model suggest that HERG inactivation is coupled to activation.
机译：HERG（一种与人类保持联系的基因）编码延迟的整流子K +通道，对心脏动作电位的正常复极化至关重要。普通药物引起的HERG突变或通道阻滞引起的极化K +电流减弱，延长了心室动作电位，增加了心律不齐和猝死的风险。 HERG在维持正常心脏电活动中的关键作用源于其异常的门控特性。与其他电压门控K +通道相反，HERG通道失活的速率比激活快，并且似乎与电压有关。为了研究与缓慢激活和快速失活相关的电压传感器运动，我们对HERG门控电流进行了表征。当使用切开的卵母细胞电压钳技术时，膜去极化引发了具有快慢成分动力学差异为100倍的门控电流。与先前研究的电压门控K +通道不同，HERG中的大部分电荷移动是持久的，这与离子电流激活的慢速一致。尽管具有相似的动力学特征，但快速灭活并非源自快速门控组件。对失活不足的突变体HERG通道和马尔可夫动力学模型的分析表明，HERG失活与激活相关。

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