蛋氨酸氧化加速电压门控钾通道中P/C型失活
Acceleration of P/C-type inactivation in voltage-gated K(+) channels by methionine oxidation.
作者信息
Chen J, Avdonin V, Ciorba M A, Heinemann S H, Hoshi T
机构信息
Department of Physiology, The University of Iowa, Iowa City, Iowa 52242 USA.
出版信息
Biophys J. 2000 Jan;78(1):174-87. doi: 10.1016/S0006-3495(00)76583-0.
Abstract
Oxidation of amino acid residues causes noticeable changes in gating of many ion channels. We found that P/C-type inactivation of Shaker potassium channels expressed in Xenopus oocytes is irreversibly accelerated by patch excision and that this effect was mimicked by application of the oxidant H(2)O(2), which is normally produced in cells by the dismutase action on the superoxide anion. The inactivation time course was also accelerated by high concentration of O(2). Substitution of a methionine residue located in the P-segment of the channel with a leucine largely eliminated the channel's sensitivity to patch excision, H(2)O(2), and high O(2). The results demonstrate that oxidation of methionine is an important regulator of P/C-type inactivation and that it may play a role in mediating the cellular responses to hypoxia/hyperoxia.
摘要
氨基酸残基的氧化会导致许多离子通道门控发生显著变化。我们发现，非洲爪蟾卵母细胞中表达的Shaker钾通道的P/C型失活会因膜片钳切除而不可逆地加速，并且这种效应可通过施加氧化剂H₂O₂来模拟，H₂O₂通常由细胞中歧化酶对超氧阴离子的作用产生。高浓度的O₂也会加速失活时间进程。用亮氨酸取代通道P段中的一个甲硫氨酸残基，在很大程度上消除了通道对膜片钳切除、H₂O₂和高浓度O₂的敏感性。结果表明，甲硫氨酸的氧化是P/C型失活的重要调节因子，并且它可能在介导细胞对缺氧/高氧的反应中发挥作用。
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