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- W3171651193 abstract "The human ether-a-go-go-related gene (hERG) encodes the rapidly activating delayed rectifier potassium channel (IKr) which is critical for repolarization of cardiac action potential. Loss of function of hERG channels due to gene mutations or drug blockade causes long QT syndrome. Presently, little is known about the restoration or enhancement of hERG channel function. In the present study, we found that muscarinic receptor agonist, carbachol, specifically increased hERG expression and IhERG, but had no effect on IKs, IEAG and IKv1.5 channels in HEK expression systems. Carbachol treatment decreased hERG-ubiquitin interaction and hERG degradation. It is known that hERG channels are degraded by the Nedd4–2, we found that disrupting the binding sites of Nedd4–2 by the Y1078A point mutation or C-terminal truncation Δ1073 mutation in hERG completely eliminated the effects of carbachol on hERG channels. Our data further indicate that carbachol treatment inhibited Nedd4–2 activity by enhancing its phosphorylation level. Another muscarinic receptor agonist, oxotremorine, increased hERG function, and the muscarinic receptor antagonist 4-DAMP abolished the effects of both carbachol and oxotremorine on hERG channels. Enhancement of hERG function by muscarinic receptor activation represents a novel pathway in hERG regulation, and this finding may have potential for the management of long QT syndrome patients. Supported by: Canadian Institutes of Health Research (CIHR)." @default.
- W3171651193 created "2021-06-22" @default.
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- W3171651193 date "2013-04-01" @default.
- W3171651193 modified "2023-09-23" @default.
- W3171651193 title "Activation of muscarinic receptor increases cardiac potassium hERG channel through phosphorylation of E3 ubiquitin ligase Nedd4–2" @default.
- W3171651193 doi "https://doi.org/10.1096/fasebj.27.1_supplement.553.14" @default.
- W3171651193 hasPublicationYear "2013" @default.
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