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Article

Functional consequences of stably expressing a mutant calsequestrin (CASQ2D307H) in the CASQ2 null background.

American journal of physiology. Heart and circulatory physiology - 1 Jan 2012

Kalyanasundaram Anuradha, Viatchenko-Karpinski Serge, Belevych Andriy E, Lacombe Veronique A, Hwang Hyun Seok, Knollmann Björn C, Gyorke Sandor, Periasamy Muthu

Abstract excerpt

The role of calsequestrin (CASQ2) in cardiac sarcoplasmic reticulum (SR) calcium (Ca(2+)) transport has gained significant attention since point mutations in CASQ2 were reported to cause ventricular arrhythmia. In the present study, we have critically evaluated the functional consequences of expressing the CASQ2(D307H) mutant protein in the CASQ2 null mouse. We recently reported that the mutant CASQ2(D307H)...

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Source

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Identifiers

PMID: 21984545
DOI: 10.1152/ajpheart.00578.2011
PMCID: PMC3334241

Genes

CASQ2

Variants

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

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Click a neighbor to travelStep 1 · 12 closest

Functional consequences of stably expressing a mutant calsequestrin (CASQ2D307H) in the CASQ2 null background.PMID 21984545Read ↗

Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

The calsequestrin mutation CASQ2D307H does not affect protein stability and targeting to the junctional sarcoplasmic reticulum but compromises its dynamic regulation of calcium buffering.Semantic proximity Read ↗

A mutation in calsequestrin, CASQ2D307H, impairs Sarcoplasmic Reticulum Ca2+ handling and causes complex ventricular arrhythmias in miceSemantic proximity Read ↗

Mechanism of calsequestrin regulation of single cardiac ryanodine receptor in normal and pathological conditions.Semantic proximity Read ↗

Calsequestrin 2 (CASQ2) mutations increase expression of calreticulin and ryanodine receptors, causing catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

The cardiac ryanodine receptor luminal Ca2+ sensor governs Ca2+ waves, ventricular tachyarrhythmias and cardiac hypertrophy in calsequestrin-null mice.Semantic proximity Read ↗

The human CASQ2 mutation K206N is associated with hyperglycosylation and altered cellular calcium handling.Semantic proximity Read ↗

Viral gene transfer rescues arrhythmogenic phenotype and ultrastructural abnormalities in adult calsequestrin-null mice with inherited arrhythmias.Semantic proximity Read ↗

Modulation of sarcoplasmic reticulum calcium release by calsequestrin in cardiac myocytes.Semantic proximity Read ↗

Proteins within the intracellular calcium store determine cardiac RyR channel activity and cardiac output.Semantic proximity Read ↗

Mice null for calsequestrin 1 exhibit deficits in functional performance and sarcoplasmic reticulum calcium handling.Semantic proximity Read ↗

Abnormal interactions of calsequestrin with the ryanodine receptor calcium release channel complex linked to exercise-induced sudden cardiac death.Semantic proximity Read ↗

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