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

Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation.

Journal of molecular and cellular cardiology - 1 Oct 2000

Wan X, Wang Q, Kirsch G E

Abstract excerpt

Ventricular fibrillation leading to sudden cardiac death can occur even in the absence of structural heart disease. One form of this so-called idiopathic ventricular fibrillation (IVF) is characterized by ST segment elevation (STE) in the electrocardiogram. Recently we found that IVF with STE is linked to mutations of SCN5A, the gene encoding the cardiac sodium channel alpha -subunit. Two types of defects were...

Read the complete abstract on PubMed

Topics

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

Share to Electrophysiology
Share to Ions
Share to NAV1.5 Voltage-Gated Sodium Channel

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

Share to Oocytes

Share to Sodium Channel Blockers

Share to Sodium Channels

Share to Ventricular Fibrillation

Share to Xenopus

Source

Identifiers

PMID: 11013131
DOI: 10.1006/jmcc.2000.1223

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

Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation.PMID 11013131Read ↗

Molecular biology of sodium channels and their role in cardiac arrhythmias.Semantic proximity Read ↗

Loss-of-function mutation of the SCN3B-encoded sodium channel {beta}3 subunit associated with a case of idiopathic ventricular fibrillation.Semantic proximity Read ↗

Novel mechanism for Brugada syndrome: defective surface localization of an SCN5A mutant (R1432G).Semantic proximity Read ↗

Genetic basis and molecular mechanism for idiopathic ventricular fibrillation.Semantic proximity Read ↗

Expression and Intracellular Localization of an <b> <i>SCN5A</i> </b> Double Mutant R1232W/T1620M Implicated in Brugada SyndromeSemantic proximity Read ↗

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

Expression and intracellular localization of an SCN5A double mutant R1232W/T1620M implicated in Brugada syndrome.Semantic proximity Read ↗

Beta-subunit-eliminated eHAP expression (BeHAPe) cells reveal new properties of the cardiac voltage-gated sodium channelSemantic 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 ↗

Human heart failure is associated with abnormal C-terminal splicing variants in the cardiac sodium channel.Semantic proximity Read ↗

Beta-subunit-eliminated eHAP expression (BeHAPe) cells reveal subunit regulation of the cardiac voltage-gated sodium channel.Semantic proximity Read ↗

Ionic Mechanisms Responsible for the Electrocardiographic Phenotype of the Brugada Syndrome Are Temperature DependentSemantic proximity Read ↗

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