Author Correction: A mechanism for CO regulation of ion channels.
Author Correction: A mechanism for CO regulation of ion channels.
复制标题
DOI：
10.1038/s41467-018-05622-6
复制
发表时间：
2018-08-17
影响因子：
16.6
通讯作者：
Raven E
中科院分区：
文献类型：
--
作者：
Kapetanaki SM;Burton MJ;Basran J;Uragami C;Moody PCE;Mitcheson JS;Schmid R;Davies NW;Dorlet P;Vos MH;Storey NM;Raven E
尽管一氧化碳（CO）具有剧毒，但它也是一种重要的细胞内信号分子。CO依赖性细胞信号传导的机制尚不清楚，但可能涉及与血红素蛋白的相互作用。CO的一个这样的作用是在离子通道调节中。在这里，我们研究了CO与KATP通道的相互作用。我们发现CO激活KATP通道，并且血红素与SUR 2A受体上的CXXHX 16 H基序结合是CO依赖性增加通道活性所必需的。光谱和动力学数据被用来量化与亚铁血红素-SUR 2A复合物的CO的相互作用。这些结果是重要的，因为它们直接将CO依赖性调节与通道上的血红素结合事件联系起来。我们使用这些信息来呈现分子水平的洞察力的动态过程，控制与血红素调节通道蛋白的相互作用的CO，我们提出了一个结构框架，了解血红素和CO之间的复杂的相互作用，在离子通道调节。
Despite being highly toxic, carbon monoxide (CO) is also an essential intracellular signalling molecule. The mechanisms of CO-dependent cell signalling are poorly defined, but are likely to involve interactions with heme proteins. One such role for CO is in ion channel regulation. Here, we examine the interaction of CO with KATPchannels. We find that CO activates KATPchannels and that heme binding to a CXXHX16H motif on the SUR2A receptor is required for the CO-dependent increase in channel activity. Spectroscopic and kinetic data were used to quantify the interaction of CO with the ferrous heme-SUR2A complex. The results are significant because they directly connect CO-dependent regulation to a heme-binding event on the channel. We use this information to present molecular-level insight into the dynamic processes that control the interactions of CO with a heme-regulated channel protein, and we present a structural framework for understanding the complex interplay between heme and CO in ion channel regulation.
影响因子：
16.6
作者：
Kapetanaki SM;Burton MJ;Basran J;Uragami C;Moody PCE;Mitcheson JS;Schmid R;Davies NW;Dorlet P;Vos MH;Storey NM;Raven E
通讯作者：
Raven E