The large conductance voltage- and Ca2+-activated K+ (BK) channel is a major ionic determinant of vascular tone, vasodilation, and blood pressure. The activity of BK channels is regulated in part by membrane presentation. Rab GTPase (Rab) regulates important cellular processes, including ion channel membrane trafficking. We hypothesize that Rab4a participates in the regulation of BK channel α-subunit (BK-α) membrane trafficking. We found that vascular BK-α interacts physically with Rab4a. Co-expression of dominant-negative Rab4a reduced BK-α surface expression, whereas that of constitutively-active Rab4a augmented BK-α surface presentation. These novel findings suggest that vascular BK channel membrane expression is regulated by Rab4a through channel membrane trafficking.

中文翻译：

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大电导的Ca2 +和电压激活的K +（BK）通道的膜运输受Rab4 GTPase调控。

大的电导电压激活和Ca2 +激活的K +（BK）通道是血管张力，血管舒张和血压的主要离子决定因素。BK通道的活性部分受到膜呈递的调节。Rab GTPase（Rab）调节重要的细胞过程，包括离子通道膜运输。我们假设Rab4a参与BK通道α亚基（BK-α）膜运输的调节。我们发现血管BK-α与Rab4a发生物理相互作用。显性负性Rab4a的共表达降低BK-α表面表达，而组成性活性Rab4a的共表达增加BK-α表面表达。这些新颖的发现表明，Rab4a通过通道膜运输来调节血管BK通道膜表达。