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Article

Calmodulin variant E140G associated with long QT syndrome impairs CaMKIIδ autophosphorylation and L-type calcium channel inactivation.

The Journal of biological chemistry - 1 Jan 2023

Prakash Ohm, Gupta Nitika, Milburn Amy, McCormick Liam, Deugi Vishvangi, Fisch Pauline, Wyles Jacob, Thomas N Lowri, Antonyuk Svetlana, Dart Caroline, Helassa Nordine

Abstract excerpt

Long QT syndrome (LQTS) is a human inherited heart condition that can cause life-threatening arrhythmia including sudden cardiac death. Mutations in the ubiquitous Ca2+-sensing protein calmodulin (CaM) are associated with LQTS, but the molecular mechanism by which these mutations lead to irregular heartbeats is not fully understood. Here, we use a multidisciplinary approach including protein biophysics,...

Topics

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Arrhythmias, Cardiac
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium Channels, L-Type
Calmodulin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Crystallography

Long QT Syndrome

Myocytes, Cardiac

Ryanodine Receptor Calcium Release Channel

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Identifiers

PMID: 36496072
DOI: 10.1016/j.jbc.2022.102777
PMCID: PMC9830374

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

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Calmodulin variant E140G associated with long QT syndrome impairs CaMKIIδ autophosphorylation and L-type calcium channel inactivation.PMID 36496072Read ↗

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Arrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca2+ channel (Cav1.2) and reduce Ca2+-dependent inactivation.Semantic proximity Read ↗

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Spectrum and Prevalence of <i>CALM1</i> -, <i>CALM2</i> -, and <i>CALM3</i> -Encoded Calmodulin Variants in Long QT Syndrome and Functional Characterization of a Novel Long QT Syndrome–Associated Calmodulin Missense Variant, E141GSemantic proximity Read ↗

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