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Article

Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation.

Journal of neurophysiology - 1 Apr 2011

Gurkiewicz Meron, Korngreen Alon, Waxman Stephen G, Lampert Angelika

Abstract excerpt

Gain-of-function mutations of the voltage-gated sodium channel (VGSC) Na(v)1.7 have been linked to human pain disorders. The mutation F1449V, located at the intracellular end of transmembrane helix S6 of domain III, induces the inherited pain syndrome erythromelalgia. A kinetic model of wild-type (WT) and F1449V Na(v)1.7 may provide a basis for predicting putative intraprotein interactions. We semiautomatically...

Topics

Action Potentials
Algorithms
Erythromelalgia
HEK293 Cells
Humans
Kidney
Markov Chains
Models, Biological
Mutation
NAV1.7 Voltage-Gated Sodium Channel
Patch-Clamp Techniques

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Sodium Channels

Stochastic Processes

Transfection

Source

Identifiers

PMID: 21289137
DOI: 10.1152/jn.00703.2010

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-21289137-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation.PMID 21289137Read ↗

Novel mutations mapping to the fourth sodium channel domain of Nav1.7 result in variable clinical manifestations of primary erythromelalgia.Semantic proximity Read ↗

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