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

The oxidation-resistant CaMKII-MM281/282VV mutation does not prevent arrhythmias in CPVT1.

Physiological reports - 1 Sept 2021

Sadredini Mani, Manotheepan Ravinea, Lehnart Stephan E, Anderson Mark E, Sjaastad Ivar, Stokke Mathis K

Abstract excerpt

Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is an inherited arrhythmogenic disorder caused by missense mutations in the cardiac ryanodine receptors (RyR2), that result in increased β-adrenoceptor stimulation-induced diastolic Ca2+ leak. We have previously shown that exercise training prevents arrhythmias in CPVT1, potentially by reducing the oxidation of Ca2+ /calmodulin-dependent protein...

Read the complete abstract on PubMed

Topics

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

Share to Calcium-Calmodulin-Dependent Protein Kinase Type 2
Share to Calcium Signaling

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

Share to Mice, Inbred C57BL

Share to Myocytes, Cardiac

Share to Oxidants

Share to Oxidation-Reduction

Share to Ryanodine Receptor Calcium Release Channel

Share to Tachycardia, Ventricular

Source

Open in PubMed Open full text

Identifiers

PMID: 34558218
DOI: 10.14814/phy2.15030
PMCID: PMC8461029

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The oxidation-resistant CaMKII-MM281/282VV mutation does not prevent arrhythmias in CPVT1.PMID 34558218Read ↗

Exercise training prevents ventricular tachycardia in CPVT1 due to reduced CaMKII-dependent arrhythmogenic Ca2+ release.Semantic proximity Read ↗

CaMKII Phosphorylation of RYR2 is Essential for Arrhythmia in CPVTSemantic proximity Read ↗

Prevention of ventricular arrhythmia and calcium dysregulation in a catecholaminergic polymorphic ventricular tachycardia mouse model carrying calsequestrin-2 mutation.Semantic proximity Read ↗

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

Ryanodine receptors and ventricular arrhythmias: emerging trends in mutations, mechanisms and therapies.Semantic proximity Read ↗

The V2475F CPVT1 mutation yields distinct RyR2 channel populations that differ in their responses to cytosolic Ca2+ and Mg2.Semantic proximity Read ↗

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

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

Characterization of a novel mutation in the cardiac ryanodine receptor that results in catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

Enhanced store overload-induced Ca2+ release and channel sensitivity to luminal Ca2+ activation are common defects of RyR2 mutations linked to ventricular tachycardia and sudden death.Semantic proximity Read ↗

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

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

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