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Article

Y1767C, a novel SCN5A mutation, induces a persistent Na+ current and potentiates ranolazine inhibition of Nav1.5 channels.

American journal of physiology. Heart and circulatory physiology - 1 Jan 2011

Huang Hai, Priori Silvia G, Napolitano Carlo, O'Leary Michael E, Chahine Mohamed

Abstract excerpt

Long QT syndrome type 3 (LQT3) has been traced to mutations of the cardiac Na(+) channel (Na(v)1.5) that produce persistent Na(+) currents leading to delayed ventricular repolarization and torsades de pointes. We performed mutational analyses of patients suffering from LQTS and characterized the biophysical properties of the mutations that we uncovered. One LQT3 patient carried a mutation in the SCN5A gene in...

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Source

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Identifiers

PMID: 21076026
DOI: 10.1152/ajpheart.00539.2010
PMCID: PMC3774256

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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