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

Biophysical defects of an SCN5A V1667I mutation associated with epinephrine-induced marked QT prolongation.

Journal of cardiovascular electrophysiology - 1 Aug 2020

Nakajima Tadashi, Dharmawan Tommy, Kawabata-Iwakawa Reika, Tamura Shuntaro, Hasegawa Hiroshi, Kobari Takashi, Kaneko Yoshiaki, Nishiyama Masahiko, Kurabayashi Masahiko

Abstract excerpt

BACKGROUND: The epinephrine infusion test (EIT) typically induces marked QT prolongation in LQT1, but not LQT3, while the efficacy of β-blocker therapy is established in LQT1, but not LQT3. We encountered an LQT3 family, with an SCN5A V1667I mutation, that exhibited epinephrine-induced marked QT prolongation. METHODS: Wild-type (WT) or V1667I-SCN5A was transiently expressed into tsA-201 cells, and whole-cell...

Read the complete abstract on PubMed

Topics

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

Share to Epinephrine
Share to Long QT Syndrome

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to NAV1.5 Voltage-Gated Sodium Channel

Source

Identifiers

PMID: 32437023
DOI: 10.1111/jce.14575

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Biophysical defects of an SCN5A V1667I mutation associated with epinephrine-induced marked QT prolongation.PMID 32437023Read ↗

Cardiac sodium channel mutation associated with epinephrine-induced QT prolongation and sinus node dysfunction.Semantic proximity Read ↗

Reduced current density, partially rescued by mexiletine, and depolarizing shift in activation of SCN5A W374G channels as a cause of severe form of Brugada syndrome.Semantic proximity Read ↗

Clinical and electrophysiological characterization of a SCN5A gain-of-function mutation associated with CPVT-like arrhythmiaSemantic proximity Read ↗

Mexiletine rescues a mixed biophysical phenotype of the cardiac sodium channel arising from the SCN5A mutation, N406K, found in LQT3 patients.Semantic proximity Read ↗

The E1784K mutation in SCN5A is associated with mixed clinical phenotype of type 3 long QT syndrome.Semantic proximity Read ↗

Enhanced fast-inactivated state stability of cardiac sodium channels by a novel voltage sensor SCN5A mutation, R1632C, as a cause of atypical Brugada syndrome.Semantic proximity Read ↗

Arrhythmogenic Biophysical Phenotype for SCN5A Mutation S1787N Depends upon Splice Variant Background and Intracellular Acidosis.Semantic proximity Read ↗

Sodium overload due to a persistent current that attenuates the arrhythmogenic potential of a novel LQT3 mutationSemantic proximity Read ↗

Contribution of sodium channel mutations to bradycardia and sinus node dysfunction in LQT3 families.Semantic proximity Read ↗

Rate-dependent QT shortening mechanism for the LQT3 deltaKPQ mutant.Semantic proximity Read ↗

Altered Na+ channels promote pause-induced spontaneous diastolic activity in long QT syndrome type 3 myocytes.Semantic proximity Read ↗

Increased early sodium current causes familial atrial fibrillation and dampens effect of flecainideSemantic proximity Read ↗

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