Non-equilibrium Gating in cardiac Na+ channels -: An original mechanism of arrhythmia
Non-equilibrium Gating in cardiac Na+ channels -: An original mechanism of arrhythmia
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DOI：
10.1161/01.cir.0000069273.51375.bd
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发表时间：
2003-05-06
期刊：
影响因子：
37.8
通讯作者：
Kass, RS
中科院分区：
文献类型：
--
作者：
Clancy, CE;Tateyama, M;Kass, RS
背景-心脏Na+通道中的许多长QT综合征（LQTS）突变导致功能增强，这是由于一部分通道未能猝发（爆发），导致去极化期间的持续电流（I-sus）。然而，一些与心律失常有因果关系的Na+通道突变不会导致使用标准膜片钳技术测量的明显功能增益。在此提出的一个例子，SCN 5A LQTS突变体I1768 V，不起作用，以增加I-sus（
Background - Many long-QT syndrome (LQTS) mutations in the cardiac Na+ channel result in a gain of function due to a fraction of channels that fail to inactivate ( burst), leading to sustained current (I-sus) during depolarization. However, some Na+ channel mutations that are causally linked to cardiac arrhythmia do not result in an obvious gain of function as measured using standard patch-clamp techniques. An example presented here, the SCN5A LQTS mutant I1768V, does not act to increase I-sus (