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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Defining the BK channel domains required for beta 1-subunit modulation
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Defining the BK channel domains required for beta 1-subunit modulation

机译：定义β1亚基调制所需的BK通道域

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摘要

in a wide variety of cell types, including neurons and smooth muscle cells, activation of the large-conductance voltage- and Ca2+-activated K+ (BK) channels causes transient membrane hyperpolarization, thereby regulating cellular excitability. Similar to other voltage-gated ion channels, BK channels, a tetramer of alpha-subunits, associate with auxiliary beta-subunits in a tissue-specific manner, modifying the channel's gating properties. The BK beta 1-subunit, which is expressed in smooth muscle, increases the apparent Ca2+ sensitivity (marked by a hyperpolarizing shift in the conductance-voltage relationship at a given Ca2+ concentration), slows macroscopic activation and deactivation, and is required for channel activation by 17 beta-estradiol. The beta 1-subunit is essential for normal regulation of vascular smooth muscle contractility and blood pressure. Little is known, however, about the molecular mechanisms of beta 1-subunit modulation of alpha-subunits. Here we show that the beta 1-subunit's modulation of the Ca2+ and 17 beta-estradiol sensitivities can be dissociated from its effects on gating kinetics by truncation of the a-subunit's extracellular N-terminal residues. The BK alpha-subunit N terminus interacts uniquely with the beta 1-subunit: beta 2 regulation of the a-subunit is unaltered by truncation of the N terminus. Although the functional interaction of alpha and beta 1 requires the N-terminal tail of alpha, the physical association requires the S1, S2, and S3 transmembrane helices of a.
机译：在包括神经元和平滑肌细胞在内的多种细胞类型中，大电导电压和Ca2 +激活的K +（BK）通道的激活会引起瞬时膜超极化，从而调节细胞的兴奋性。与其他电压门控离子通道相似，BK通道是α亚基的四聚体，以组织特异性方式与辅助β亚基缔合，从而改变了通道的门控特性。在平滑肌中表达的BK beta 1亚基增加了表观Ca2 +敏感性（以给定Ca2 +浓度下电导-电压关系的超极化位移为特征），减慢了宏观激活和失活，并且需要通道激活通过17β-雌二醇。 β1亚基对于正常调节血管平滑肌收缩力和血压至关重要。然而，对β-亚基调节α-亚基的分子机制知之甚少。在这里，我们表明，β1亚基对Ca2 +和17β-雌二醇敏感性的调节可以通过截断a亚基的胞外N端残基而使其对门控动力学的影响解离。 BKα亚基N末端与β1亚基唯一相互作用：α亚基的β2调节不会由于N末端的截断而改变。尽管alpha和beta 1的功能相互作用需要alpha的N末端尾部，但物理缔合需要a的S1，S2和S3跨膜螺旋。

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