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Cardiac sarcolemmal K(ATP) channels: Latest twists in a questing tale!

机译:心脏肌膜K(ATP)通道:寻味故事的最新转折!

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Reconstitution of K(ATP) channel activity from coexpression of members of the pore-forming inward rectifier gene family (Kir6.1, KCNJ8, and Kir6.2 KCNJ11) with sulfonylurea receptors (SUR1, ABCC8, and SUR2, ABCC9) of the ABCC protein sub-family, has led to the elucidation of many details of channel gating and pore properties, as well as the essential roles of Kir6.2 and SUR2 subunits in generating cardiac ventricular K(ATP). However, despite this extensive body of knowledge, there remain significant holes in our understanding of the physiological role of the cardiac K(ATP) channel, and surprising new findings keep emerging. Recent findings from genetically modified animals include the apparent insensitivity of cardiac sarcolemmal channels to nucleotide levels, and unenvisioned complexities of the subunit make-up of the cardiac channels. This topical review focuses on these new findings and considers their implications.
机译:由ABCC的磺酰脲受体(SUR1,ABCC8和SUR2,ABCC9)共表达孔形成的内向整流基因家族成员(Kir6.1,KCNJ8和Kir6.2 KCNJ11)重建K(ATP)通道活性蛋白亚家族,导致阐明了许多通道门控和孔特性的细节,以及Kir6.2和SUR2亚基在产生心脏心室K(ATP)中的重要作用。但是,尽管拥有广泛的知识,但我们对心脏K(ATP)通道的生理作用的理解仍存在重大漏洞,令人惊讶的新发现不断出现。转基因动物的最新发现包括心脏肌膜通道对核苷酸水平的明显不敏感性,以及预想不到的心脏通道亚基组成的复杂性。这次主题回顾着重于这些新发现并考虑了它们的含义。

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