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.
MeSH terms
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Animals
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Cattle
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Cell Line
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Electrophysiology
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Estradiol / genetics
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Estradiol / metabolism*
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Humans
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Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
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Large-Conductance Calcium-Activated Potassium Channel beta Subunits
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Large-Conductance Calcium-Activated Potassium Channels
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Patch-Clamp Techniques
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Potassium Channels / metabolism*
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Potassium Channels, Calcium-Activated*
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Protein Binding
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RNA, Messenger
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Rats
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Xenopus laevis
Substances
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KCNMA1 protein, human
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Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
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Large-Conductance Calcium-Activated Potassium Channel beta Subunits
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Large-Conductance Calcium-Activated Potassium Channels
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Potassium Channels
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Potassium Channels, Calcium-Activated
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RNA, Messenger
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Estradiol