K2P potassium channels, mysterious and paradoxically exciting.

K2P potassium channels, mysterious and paradoxically exciting.
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DOI:
10.1126/scisignal.2002225
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发表时间:
2011-07-26
期刊:
影响因子:
7.3
通讯作者:
Goldstein SA
Goldstein SA
中科院分区:
生物学1区
文献类型:
--
作者:
Goldstein SA

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新的证据表明,常见的电解质紊乱低钾血症可以诱导通常对K+具有选择性的K2 P1通道打破规则并传导Na+。这种反抗行为导致心脏中许多细胞的反常去极化,增加致命性心律失常的风险。这项新的研究解决了50年前发现的一个谜团,并提出了一系列新的谜题。在这里,我将讨论如何K2 P1可能实现这一愿望,通过稳定的住宅的K+选择性过滤器在Na+导电状态之间的开放和C-非活性配置,并预测其他K+通道和环境刺激将被发现产生相同的兴奋性不当行为。
New evidence reveals that the common electrolyte disorder hypokalemia can induce K2P1 channels that are normally selective for K+ to break the rules and conduct Na+. This defiant behavior leads to paradoxical depolarization of many cells in the heart, increasing the risk for lethal arrhythmia. The new research resolves a mystery uncovered 50 years ago and bestows an array of new riddles. Here, I discuss how K2P1 might achieve this alchemy—through stable residence of the K+ selectivity filter in a Na+-conductive state between its open and C-inactive configurations—and predict that other K+ channels and environmental stimuli will be discovered to produce the same excitatory misconduct.
DOI: 10.1085/jgp.70.6.725
发表时间: 1977-12
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