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Article

The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.

The Journal of physiology - 15 Oct 2012

Song Weihua, Xiao Yucheng, Chen Hanying, Ashpole Nicole M, Piekarz Andrew D, Ma Peilin, Hudmon Andy, Cummins Theodore R, Shou Weinian

Abstract excerpt

The deletion of phenylalanine 1486 (F1486del) in the human cardiac voltage-gated sodium channel (hNav1.5) is associated with fatal long QT (LQT) syndrome. In this study we determined how F1486del impairs the functional properties of hNav1.5 and alters action potential firing in heterologous expression systems (human embryonic kidney (HEK) 293 cells) and their native cardiomyocyte background. Cells expressing...

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Identifiers

PMID: 22826127
DOI: 10.1113/jphysiol.2012.235374
PMCID: PMC3497567

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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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