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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Molecular basis of fast inactivation in voltage and Ca2+-activated K+ channels: A transmembrane beta-subunit homolog
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Molecular basis of fast inactivation in voltage and Ca2+-activated K+ channels: A transmembrane beta-subunit homolog

机译：电压和Ca2 +激活的K +通道快速失活的分子基础：跨膜β亚基同系物

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摘要

Voltage-dependent and calcium- sensitive K+ (MaxiK) channels are key regulators of neuronal excitability, secretion, and vascular tone because of their ability to sense transmembrane voltage and intracellular Caz2+. In most tis- sues, their stimulation results in a noninactivating hyperpo- larizing K+ current that reduces excitability. In addition to noninactivating MaxiK currents, an inactivating MaxiK chan- ncl Phenotype is found in cells like chromaffin cells and hippocampal neurons. The molecular determinants underly- ing inactivating MaxiK channels remain unknown. Herein, we report a transmembrane beta subunit (beta 2) that yields inactivat- ing MaxiK currents on coexpression with the pore-forming alpha subunit of MaxiK channels. Intracellular application of tryp- sin as well as deletion of 19 N-terminal amino acids of the beta 2 subunit abolished inactivation of the alpha subunit. Conversely, fusion of these N-terminal amino acids to the noninactivating smooth muscle beta l subunit leads to an inactivating phenotype of MaxiK channels. Furthermore, addition of a synthetic N-terminal peptide of the beta2 subunit causes inactivation of the MaxiK channel a subunit by occluding its K+-conducting pore resembling the inactivation caused by the ``ball'' peptide in voltage-dependent K+ channels. Thus, the inactivating phenotype of MaxiK channels in native tissues can result from the association with different beta subunits.
机译：电压依赖性和钙敏感性K +（MaxiK）通道是神经元兴奋性，分泌和血管紧张度的关键调节剂，因为它们具有感应跨膜电压和细胞内Caz2 +的能力。在大多数情况下，它们的刺激会导致非灭活的超极化K +电流，从而降低兴奋性。除了非灭活的MaxiK电流外，在嗜铬细胞和海马神经元等细胞中也发现了灭活的MaxiK通道表型。灭活MaxiK通道的分子决定因素仍然未知。在本文中，我们报道了跨膜β亚基（β2）在与MaxiK通道的成孔α亚基共表达时产生失活的MaxiK电流。胰蛋白酶的细胞内施用以及β2亚基的19个N末端氨基酸的缺失消除了α亚基的失活。相反，这些N末端氨基酸与非灭活的平滑肌β1亚基的融合导致MaxiK通道的灭活表型。此外，添加beta2亚基的合成N端肽会导致MaxiK通道亚基失活，原因是它的K +传导孔被封闭，类似于电压依赖性K +通道中``球''肽引起的失活。因此，天然组织中MaxiK通道的失活表型可能是由于与不同的β亚基缔合所致。

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