Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Sodium channel slow inactivation interferes with open channel block.

Scientific reports - 13 May 2016

Hampl Martin, Eberhardt Esther, O'Reilly Andrias O, Lampert Angelika

Abstract excerpt

Mutations in the voltage-gated sodium channel Nav1.7 are linked to inherited pain syndromes such as erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD). PEPD mutations impair Nav1.7 fast inactivation and increase persistent currents. PEPD mutations also increase resurgent currents, which involve the voltage-dependent release of an open channel blocker. In contrast, IEM mutations, whenever tested,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Action Potentials
Share to Erythromelalgia
Share to HEK293 Cells

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

Share to NAV1.6 Voltage-Gated Sodium Channel

Share to NAV1.7 Voltage-Gated Sodium Channel

Share to Patch-Clamp Techniques

Share to Rectum

Source

Open in PubMed Open full text

Identifiers

PMID: 27174182
DOI: 10.1038/srep25974
PMCID: PMC4865801

Genes

PEPD

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

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sodium channel slow inactivation interferes with open channel block.PMID 27174182Read ↗

Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation.Semantic proximity Read ↗

Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.Semantic proximity Read ↗

Novel SCN9A mutations underlying extreme pain phenotypes: unexpected electrophysiological and clinical phenotype correlations.Semantic proximity Read ↗

NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders.Semantic proximity Read ↗

Slow inactivation in voltage-gated sodium channels: molecular substrates and contributions to channelopathies.Semantic proximity Read ↗

Cold and warmth intensify pain-linked sodium channel gating effects and persistent currentsSemantic proximity Read ↗

Deletion mutation of sodium channel NaV1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitabilitySemantic proximity Read ↗

Erythromelalgia mutation L823R shifts activation and inactivation of threshold sodium channel Nav1.7 to hyperpolarized potentials.Semantic proximity Read ↗

Pain disorders and erythromelalgia caused by voltage-gated sodium channel mutations.Semantic proximity Read ↗

Mechanisms of sodium channel inactivation.Semantic proximity Read ↗

Lidocaine reduces the transition to slow inactivation in Na(v)1.7 voltage-gated sodium channels.Semantic proximity Read ↗

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

⌁Select a neighboring publication to make it the new centre.