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Article

Arrhythmogenic calmodulin mutations disrupt intracellular cardiomyocyte Ca2+ regulation by distinct mechanisms.

Journal of the American Heart Association - 23 Jun 2014

Yin Guo, Hassan Faisal, Haroun Ayman R, Murphy Lisa L, Crotti Lia, Schwartz Peter J, George Alfred L, Satin Jonathan

Abstract excerpt

BACKGROUND: Calmodulin (CaM) mutations have been identified recently in subjects with congenital long QT syndrome (LQTS) or catecholaminergic polymorphic ventricular tachycardia (CPVT), but the mechanisms responsible for these divergent arrhythmia-susceptibility syndromes in this context are unknown. We tested the hypothesis that LQTS-associated CaM mutants disrupt Ca2+ homeostasis in developing cardiomyocytes...

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Source

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Identifiers

PMID: 24958779
DOI: 10.1161/JAHA.114.000996
PMCID: PMC4309107

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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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