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雌二醇与β亚基结合导致大电导钙激活钾通道(hSlo)急性激活。

Acute activation of Maxi-K channels (hSlo) by estradiol binding to the beta subunit.

作者信息

Valverde M A, Rojas P, Amigo J, Cosmelli D, Orio P, Bahamonde M I, Mann G E, Vergara C, Latorre R

机构信息

Departament de Ciències Experimentals i de la Salut, Universidad Pompeu Fabra, C/Doctor Aiguader 80, 08003 Barcelona, Spain.

出版信息

Science. 1999 Sep 17;285(5435):1929-31. doi: 10.1126/science.285.5435.1929.

Abstract

Maxi-K channels consist of a pore-forming alpha subunit and a regulatory beta subunit, which confers the channel with a higher Ca(2+) sensitivity. Estradiol bound to the beta subunit and activated the Maxi-K channel (hSlo) only when both alpha and beta subunits were present. This activation was independent of the generation of intracellular signals and could be triggered by estradiol conjugated to a membrane-impenetrable carrier protein. This study documents the direct interaction of a hormone with a voltage-gated channel subunit and provides the molecular mechanism for the modulation of vascular smooth muscle Maxi-K channels by estrogens.

摘要

大电导钙激活钾通道(Maxi-K通道)由一个形成孔道的α亚基和一个调节性β亚基组成,后者赋予该通道更高的钙敏感性。仅当α亚基和β亚基同时存在时,与β亚基结合的雌二醇才能激活Maxi-K通道(hSlo)。这种激活不依赖于细胞内信号的产生,并且可由与膜不可渗透的载体蛋白偶联的雌二醇触发。本研究记录了一种激素与电压门控通道亚基的直接相互作用,并提供了雌激素调节血管平滑肌Maxi-K通道的分子机制。

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