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

Loss of Nav1.5 expression and function in murine atria containing the RyR2-P2328S gain-of-function mutation.

Cardiovascular research - 1 Sept 2013

King James H, Wickramarachchi Chandu, Kua Krystine, Du Yuan, Jeevaratnam Kamalan, Matthews Hugh R, Grace Andrew A, Huang Christopher L-H, Fraser James A

Abstract excerpt

AIMS: Recent studies reported slowed conduction velocity (CV) in murine hearts homozygous for the gain-of-function RyR2-P2328S mutation (RyR2(S/S)) and associated this with an increased incidence of atrial and ventricular arrhythmias. The present experiments determined mechanisms contributing to the reduced atrial CV. METHODS AND RESULTS: The determinants of CV were investigated in murine RyR2(S/S) hearts and...

Read the complete abstract on PubMed

Topics

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

Share to Arrhythmias, Cardiac
Share to Connexin 43

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

Share to Connexins

Share to Gap Junction alpha-5 Protein

Share to Heart Atria

Share to Heart Conduction System

Share to NAV1.5 Voltage-Gated Sodium Channel

Share to Ryanodine Receptor Calcium Release Channel

Source

Identifiers

PMID: 23723061
DOI: 10.1093/cvr/cvt141

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

Loss of Nav1.5 expression and function in murine atria containing the RyR2-P2328S gain-of-function mutation.PMID 23723061Read ↗

Slowed conduction and ventricular tachycardia after targeted disruption of the cardiac sodium channel gene Scn5a.Semantic proximity Read ↗

Flecainide exerts paradoxical effects on sodium currents and atrial arrhythmia in murine RyR2-P2328S hearts.Semantic proximity Read ↗

The Kir2.1E299V mutation increases atrial fibrillation vulnerability while protecting the ventricles against arrhythmias in a mouse model of short QT syndrome type 3.Semantic proximity Read ↗

TGF-β1-mediated fibrosis and ion channel remodeling are key mechanisms in producing the sinus node dysfunction associated with SCN5A deficiency and aging.Semantic proximity Read ↗

Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias.Semantic proximity Read ↗

Cardiac Sodium Channel Mutations: Why so Many Phenotypes?Semantic proximity Read ↗

Knock-in gain-of-function sodium channel mutation prolongs atrial action potentials and alters atrial vulnerability.Semantic proximity Read ↗

Arrhythmias precede cardiomyopathy and remodeling of Ca2+ handling proteins in a novel model of long QT syndrome.Semantic proximity Read ↗

Mouse Model of Human Congenital Heart Disease: Progressive Atrioventricular Block Induced by a Heterozygous Nkx2-5 Homeodomain Missense Mutation.Semantic proximity Read ↗

A Novel SCN5A Variant Associated with Abnormal Repolarization, Atrial Fibrillation, and Reversible Cardiomyopathy.Semantic proximity Read ↗

Genetically determined differences in sodium current characteristics modulate conduction disease severity in mice with cardiac sodium channelopathy.Semantic proximity Read ↗

Variable Na(v)1.5 protein expression from the wild-type allele correlates with the penetrance of cardiac conduction disease in the Scn5a(+/-) mouse model.Semantic proximity Read ↗

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