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Article

Elementary mechanisms of calmodulin regulation of NaV1.5 producing divergent arrhythmogenic phenotypes.

Proceedings of the National Academy of Sciences of the United States of America - 25 May 2021

Kang Po Wei, Chakouri Nourdine, Diaz Johanna, Tomaselli Gordon F, Yue David T, Ben-Johny Manu

Abstract excerpt

In cardiomyocytes, NaV1.5 channels mediate initiation and fast propagation of action potentials. The Ca2+-binding protein calmodulin (CaM) serves as a de facto subunit of NaV1.5. Genetic studies and atomic structures suggest that this interaction is pathophysiologically critical, as human mutations within the NaV1.5 carboxy-terminus that disrupt CaM binding are linked to distinct forms of life-threatening...

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Identifiers

PMID: 34021086
DOI: 10.1073/pnas.2025085118
PMCID: PMC8166197

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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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