Acute Activation of Maxi-K Channels ( hSlo ) by Estradiol Binding to the β Subunit

Author:

Valverde Miguel A.1,Rojas Patricio2,Amigo Julio2,Cosmelli Diego2,Orio Patricio2,Bahamonde Maria I.2,Mann Giovanni E.3,Vergara Cecilia2,Latorre Ramon24

Affiliation:

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

2. Departmento de Biologı́a, Facultad de Ciencias, Universidad de Chile, Casilla 653, Santiago, Chile, and Centro de Estudios Cientificos de Santiago, Casilla 16443, Santiago 9, Chile.

3. Centre for Cardiovascular Biology and Medicine, School of Biomedical Sciences, King's College London, London SE1 9RT, UK.

4. Department of Anesthesiology, University of California Los Angeles, Los Angeles, CA 90095-1778, USA.

Abstract

Maxi-K channels consist of a pore-forming α subunit and a regulatory β subunit, which confers the channel with a higher Ca 2+ sensitivity. Estradiol bound to the β subunit and activated the Maxi-K channel ( hSlo ) only when both α and β 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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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