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Article

Uncoupling sodium channel dimers restores the phenotype of a pain-linked Nav 1.7 channel mutation.

British journal of pharmacology - 1 Oct 2020

Rühlmann Annika H, Körner Jannis, Hausmann Ralf, Bebrivenski Nikolay, Neuhof Christian, Detro-Dassen Silvia, Hautvast Petra, Benasolo Carène A, Meents Jannis, Machtens Jan-Philipp, Schmalzing Günther, Lampert Angelika

Abstract excerpt

BACKGROUND AND PURPOSE: The voltage-gated sodium channel Nav 1.7 is essential for adequate perception of painful stimuli. Mutations in the encoding gene, SCN9A, cause various pain syndromes in humans. The hNav 1.7/A1632E channel mutant causes symptoms of erythromelalgia and paroxysmal extreme pai...

Topics

Erythromelalgia
Humans
Mutation
NAV1.7 Voltage-Gated Sodium Channel
Pain
Phenotype

Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 32663327
DOI: 10.1111/bph.15196
PMCID: PMC7484505

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-32663327-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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Uncoupling sodium channel dimers restores the phenotype of a pain-linked Nav 1.7 channel mutation.PMID 32663327Read ↗

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