Yang Y, Yan Y, Sigworth F J
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA.
J Gen Physiol. 1997 Jun;109(6):779-89. doi: 10.1085/jgp.109.6.779.
The mutation W434F produces an apparently complete block of potassium current in Shaker channels expressed in Xenopus oocytes. Tandem tetrameric constructs containing one or two subunits with this mutation showed rapid inactivation, although the NH2-terminal inactivation domain was absent from these constructs. The inactivation showed a selective dependence on external cations and was slowed by external TEA; these properties are characteristic of C-type inactivation. Inactivation was, however, incompletely relieved by hyperpolarization, suggesting the presence of a voltage-independent component. The hybrid channels had near-normal conductance and ion selectivity. Single-channel recordings from patches containing many W434F channels showed occasional channel openings, consistent with open probabilities of 10(-5) or less. We conclude that the W434F mutation produces a channel that is predominantly found in an inactivated state.
W434F突变在非洲爪蟾卵母细胞中表达的Shaker通道中导致钾电流明显完全阻断。含有一个或两个带有此突变亚基的串联四聚体构建体表现出快速失活，尽管这些构建体中不存在NH2末端失活结构域。失活表现出对外部阳离子的选择性依赖，并且被外部TEA减慢；这些特性是C型失活的特征。然而，超极化并不能完全消除失活，这表明存在电压非依赖性成分。杂合通道具有接近正常的电导和离子选择性。来自含有许多W434F通道的膜片的单通道记录偶尔显示通道开放，开放概率为10（-5）或更低。我们得出结论，W434F突变产生的通道主要处于失活状态。
