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Article

Dysfunctional potassium channel subunit interaction as a novel mechanism of long QT syndrome.

Heart rhythm - 1 May 2013

Hoosien Michael, Ahearn Mary Ellen, Myerburg Robert J, Pham Thai V, Miller Todd E, Smets Marcel J, Baumbach-Reardon Lisa, Young Ming-Lon, Farooq Amjad, Bishopric Nanette H

Abstract excerpt

BACKGROUND: The slowly-activating delayed rectifier current IKs contributes to repolarization of the cardiac action potential, and is composed of a pore-forming α-subunit, KCNQ1, and a modulatory β-subunit, KCNE1. Mutations in either subunit can cause long QT syndrome, a potentially fatal arrhythmic disorder. How KCNE1 exerts its extensive control over the kinetics of IKs remains unresolved OBJECTIVE: To evaluate...

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Source

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Identifiers

PMID: 23291057
DOI: 10.1016/j.hrthm.2012.12.033
PMCID: PMC4770260

Genes

KCNQ1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Dysfunctional potassium channel subunit interaction as a novel mechanism of long QT syndrome.PMID 23291057Read ↗

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