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Article

RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR).

Proceedings of the National Academy of Sciences of the United States of America - 31 Aug 2004

Jiang Dawei, Xiao Bailong, Yang Dongmei, Wang Ruiwu, Choi Philip, Zhang Lin, Cheng Heping, Chen S R Wayne

Abstract excerpt

The cardiac ryanodine receptor (RyR2) governs the release of Ca2+ from the sarcoplasmic reticulum, which initiates muscle contraction. Mutations in RyR2 have been linked to ventricular tachycardia (VT) and sudden death, but the precise molecular mechanism is unclear. It is known that when the sar...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 15322274
DOI: 10.1073/pnas.0402388101
PMCID: PMC516517

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-15322274-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR).PMID 15322274Read ↗

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