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

Conduction slowing contributes to spontaneous ventricular arrhythmias in intrinsically active murine RyR2-P2328S hearts.

Journal of cardiovascular electrophysiology - 1 Feb 2013

Zhang Yanmin, Wu JingJing, Jeevaratnam Kamalan, King James H, Guzadhur Laila, Ren XiaoLei, Grace Andrew A, Lei Ming, Huang Christopher L-H, Fraser James A

Abstract excerpt

INTRODUCTION: The familial condition catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by episodic bidirectional ventricular tachycardia (BVT), polymorphic ventricular tachycardia (PVT), and ventricular fibrillation following adrenergic challenge. It is associated with mutations involving the cardiac ryanodine receptor (RyR2). METHODS AND RESULTS: We explored for a slowing of...

Read the complete abstract on PubMed

Topics

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

Share to Genetic Predisposition to Disease
Share to Heart Conduction System

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Transgenic

Share to Neural Conduction

Share to Polymorphic Catecholaminergic Ventricular Tachycardia

Share to Ryanodine Receptor Calcium Release Channel

Share to Tachycardia, Ventricular

Source

Identifiers

PMID: 23131176
DOI: 10.1111/jce.12015

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Conduction slowing contributes to spontaneous ventricular arrhythmias in intrinsically active murine RyR2-P2328S hearts.PMID 23131176Read ↗

Acute atrial arrhythmogenicity and altered Ca(2+) homeostasis in murine RyR2-P2328S hearts.Semantic proximity Read ↗

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

Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation.Semantic proximity Read ↗

Paradoxical effect of increased diastolic Ca(2+) release and decreased sinoatrial node activity in a mouse model of catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

Arrhythmogenesis in a catecholaminergic polymorphic ventricular tachycardia mutation that depresses ryanodine receptor function.Semantic proximity Read ↗

Protein expression profiles in murine ventricles modeling catecholaminergic polymorphic ventricular tachycardia: effects of genotype and sex.Semantic proximity Read ↗

Physiological consequences of the P2328S mutation in the ryanodine receptor (RyR2) gene in genetically modified murine hearts.Semantic proximity Read ↗

Increased Ca2+ sensitivity of the ryanodine receptor mutant RyR2R4496C underlies catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

Na+-dependent SR Ca2+ overload induces arrhythmogenic events in mouse cardiomyocytes with a human CPVT mutation.Semantic proximity Read ↗

Heterogeneity of ryanodine receptor dysfunction in a mouse model of catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

Cardiac ryanodine receptor calcium release deficiency syndrome.Semantic proximity Read ↗

In situ confocal imaging in intact heart reveals stress-induced Ca(2+) release variability in a murine catecholaminergic polymorphic ventricular tachycardia model of type 2 ryanodine receptor(R4496C+/-) mutation.Semantic proximity Read ↗

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