Extracellular redox sensitivity of Kv1.2 potassium channels.
Extracellular redox sensitivity of Kv1.2 potassium channels.
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KV1.2钾通道的细胞外氧化还原敏感性。
DOI：
10.1038/s41598-017-08718-z
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发表时间：
2017-08-22
影响因子：
4.6
通讯作者：
Kurata HT
中科院分区：
文献类型：
--
作者：
Baronas VA;Yang RY;Kurata HT
Kv1.2是神经系统中一个重要的钾通道亚型，是研究离子通道功能的重要结构模板。然而，由于由未知机制调节的选通模式转变，Kv1.2的电压依赖表现出显著的细胞到细胞的变化。我们报告说，这种可变的行为受到细胞外氧化还原环境的调节。暴露于还原剂可促进门控特性向抑制开放的门控模式转变，并使通道在重复的去极化过程中表现出明显的使用依赖性激活。这种对细胞外氧化还原电位的敏感性在其他KV1通道中不存在，但在含有Kv1.2亚基的异构体通道中明显存在，并与已报道的细胞外氧化还原对的生理范围重叠。对候选半胱氨酸残基的诱变不能消除氧化还原敏感性。因此，我们认为外部的，氧化还原敏感的结合伙伴赋予了这些特性。
Kv1.2 is a prominent potassium channel subtype in the nervous system and serves as an important structural template for investigation of ion channel function. However, Kv1.2 voltage-dependence exhibits dramatic cell-to-cell variability due to a gating mode shift that is regulated by an unknown mechanism. We report that this variable behavior is regulated by the extracellular redox environment. Exposure to reducing agents promotes a shift in gating properties towards an ‘inhibited’ gating mode that resists opening, and causes channels to exhibit pronounced use-dependent activation during trains of repetitive depolarizations. This sensitivity to extracellular redox potential is absent in other Kv1 channels, but is apparent in heteromeric channels containing Kv1.2 subunits, and overlaps with the reported physiological range of extracellular redox couples. Mutagenesis of candidate cysteine residues fails to abolish redox sensitivity. Therefore, we suggest that an extrinsic, redox-sensitive binding partner imparts these properties.
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影响因子：
48
作者：
Gutscher, Marcus;Pauleau, Anne-Laure;Dick, Tobias P.
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