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Article

Calmodulin D133H Disrupts Cav1.2 and Kv7.1 Regulation to Prolong Cardiac Action Potentials in Long QT Syndrome.

Cells - 11 Nov 2025

Gupta Nitika, McCormick Liam F, Richards Ella M B, Wadmore Kirsty, Morris Rachael, Morris Vanessa S, Kirilenko Pavel, Fowler Ewan D, Dart Caroline, Helassa Nordine

Abstract excerpt

Calmodulin (CaM) plays a central role in cardiac excitation-contraction coupling by regulating ion channels, including the L-type calcium (Ca2+) channel Cav1.2 and the voltage-gated potassium (K+) channel Kv7.1. Mutations in CaM are linked to severe arrhythmogenic disorders such as Long QT syndrome (LQTS), yet the molecular mechanisms remain incompletely understood. Here, we investigate the structural and...

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Topics

Calmodulin
Long QT Syndrome
Humans
Action Potentials
Calcium Channels, L-Type
Calcium

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

KCNQ1 Potassium Channel

HEK293 Cells

Mutation

Animals

Source

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Identifiers

PMID: 41294816
DOI: 10.3390/cells14221763
PMCID: PMC12651261

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