ArticleThe Journal of clinical investigation2007
Chain-reaction Ca(2+) signaling in the heart.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Functional characterization of CaVα2δ mutations associated with sudden cardiac death.The Journal of biological chemistry · 2015Article
- Store-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling.Journal of molecular and cellular cardiology · 2013Review
- Sildenafil and FDP-Sr attenuate diabetic cardiomyopathy by suppressing abnormal expression of myocardial CASQ2, FKBP12.6, and SERCA2a in rats.Acta pharmacologica Sinica · 2011Article
- Subcellular Ca2+ signaling in the heart: the role of ryanodine receptor sensitivity.The Journal of general physiology · 2010Article
- Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity.Pharmacology & therapeutics · 2010Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in Ca(2+) -handling proteins in the heart have been linked to exercise-induced sudden cardiac death. The best characterized of these have been mutations in the cardiac Ca(2+) release channel known as the ryanodine receptor type 2 (RyR2). RyR2 mutations cause "leaky" channels, resulting in diastolic Ca(2+) leak from the sarcoplasmic reticulum (SR) that can trigger fatal cardiac arrhythmias during stress. In this issue of the JCI, Song et al. show that mutations in the SR Ca(2+)-binding protein calsequestrin 2 (CASQ2) in mice result not only in reduced CASQ2 expression but also in a surprising, compensatory elevation in expression of both the Ca(2+)-binding protein calreticulin and RyR2, culminating in premature Ca(2+) release from cardiac myocytes and stress-induced arrhythmia (see the related article beginning on page 1814). In the context of these findings and other recent reports studying CASQ2 mutations, we discuss how CASQ2 influences the properties of Ca(2+)-dependent regulation of RyR2 and how this contributes to cardiac arrhythmogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.