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Gating control of the cardiac sodium channel Nav1.5 by its β3-subunit involves distinct roles for a transmembrane glutamic acid and the extracellular domain
The auxiliary β3-subunit is an important functional regulator of the cardiac sodium channel Nav1.5, and some β3 mutations predispose …
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A Molecularly Detailed NaV1.5 Model Reveals a New Class I Antiarrhythmic Target
Antiarrhythmic treatment strategies remain suboptimal due to our inability to predict how drug interactions with ion channels will …
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Predicting patient response to the antiarrhythmic mexiletine based on genetic variation: Personalized medicine for long QT syndrome
Rationale: Mutations in the SCN5A gene, encoding the α subunit of the Nav1.5 channel, cause a life-threatening form of cardiac …
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Mechanisms and models of cardiac sodium channel inactivation
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Mechanisms of noncovalent β subunit regulation of NaV channel gating
Voltage-gated Na+ (NaV) channels comprise a macromolecular complex whose components tailor channel function. Key components are the …
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Regulation of Na+ channel inactivation by the DIII and DIV voltage-sensing domains
Functional eukaryotic voltage-gated Na+ (NaV) channels comprise four domains (DI–DIV), each containing six membrane-spanning segments …
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Depolarization of the conductance-voltage relationship in the NaV1.5 mutant, E1784K, is due to altered fast inactivation
© 2017 Peters et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which …
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A novel NaV1.5 voltage sensor mutation associated with severe atrial and ventricular arrhythmias
Background Inherited autosomal dominant mutations in cardiac sodium channels (NaV1.5) cause various arrhythmias, such as long QT …
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Molecular motions that shape the cardiac action potential : Insights from voltage clamp fl uorometry
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Direct measurement of cardiac Na+ channel conformations reveals molecular pathologies of inherited mutations
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