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Article

Mutant voltage-gated Na+ channels can exert a dominant negative effect through coupled gating.

American journal of physiology. Heart and circulatory physiology - 1 Nov 2018

Clatot Jérôme, Zheng Yang, Girardeau Aurore, Liu Haiyan, Laurita Kenneth R, Marionneau Céline, Deschênes Isabelle

Abstract excerpt

Mutations in voltage-gated Na+ channels have been linked to several channelopathies leading to a wide variety of diseases including cardiac arrhythmias, epilepsy, and myotonia. We have previously demonstrated that voltage-gated Na+ channel (Nav)1.5 trafficking-deficient mutant channels could lead to a dominant negative effect by impairing trafficking of the wild-type (WT) channel. We also reported that...

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Identifiers

PMID: 30118344
DOI: 10.1152/ajpheart.00721.2017
PMCID: PMC6297814

Provenance

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.

Related research

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Mutant voltage-gated Na+ channels can exert a dominant negative effect through coupled gating.PMID 30118344Read ↗

Trafficking and Gating Cooperation Between Deficient Nav1.5-mutant Channels to Rescue INa.Semantic proximity Read ↗

The β1-subunit of Na(v)1.5 cardiac sodium channel is required for a dominant negative effect through α-α interaction.Semantic proximity Read ↗

Dominant-negative effect of SCN5A N-terminal mutations through the interaction of Nav1.5 α-subunitsSemantic proximity Read ↗

p.D1690N Nav1.5 rescues p.G1748D mutation gating defects in a compound heterozygous Brugada syndrome patient.Semantic proximity Read ↗

Phenotypic Severity of SCN5A-Related Bradycardia Is Independent of Dominant-Negative and Coupled Gating Effects.Semantic proximity Read ↗

Multiple loss-of-function mechanisms contribute to SCN5A-related familial sick sinus syndrome.Semantic proximity Read ↗

Phenotypic Severity of <i>SCN5A</i> Related Bradycardia is Independent of Dominant-Negative and Coupled Gating EffectsSemantic proximity Read ↗

Nav1.5 channels can reach the plasma membrane through distinct N-glycosylation states.Semantic proximity Read ↗

Negative-dominance phenomenon with genetic variants of the cardiac sodium channel Nav1.5.Semantic proximity Read ↗

Trafficking and localisation to the plasma membrane of Nav 1.5 promoted by the β2 subunit is defective due to a β2 mutation associated with Brugada syndrome.Semantic proximity Read ↗

hERG 1a LQT2 C-terminus truncation mutants display hERG 1b-dependent dominant negative mechanisms.Semantic proximity Read ↗

SCN5A polymorphism restores trafficking of a Brugada syndrome mutation on a separate gene.Semantic proximity Read ↗

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