ArticleThe Journal of general physiology2013
Mechanism of calsequestrin regulation of single cardiac ryanodine receptor in normal and pathological conditions.
Article in The Journal of general physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 63 citations in OpenAlex.
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- Calcium arrhythmogenicity of Purkinje fibers: importance of the animal model.Frontiers in physiology · 2025Review
- Isolated Cardiac Ryanodine Receptor Function Varies Between Mammals.The Journal of membrane biology · 2024Article
- Comprehensive Analysis of Key Endoplasmic Reticulum Stress-Related Genes and Immune Infiltrates in Stanford Type A Aortic Dissection.Anatolian journal of cardiology · 2024Article
- The Dysfunction of CaInternational journal of molecular sciences · 2023Review
- EuBiophysical journal · 2023Article
- Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Review
- SNTA1-deficient human cardiomyocytes demonstrate hypertrophic phenotype and calcium handling disorder.Stem cell research & therapy · 2022Article
- The Sarcoplasmic Reticulum of Skeletal Muscle Cells: A Labyrinth of Membrane Contact Sites.Biomolecules · 2022Review
- Calsequestrin 2 overexpression in breast cancer increases tumorigenesis and metastasis by modulating the tumor microenvironment.Molecular oncology · 2022Article
- Association of decreased triadin expression level with apoptosis of dopaminergic cells in Parkinson's disease mouse model.BMC neuroscience · 2021Article
- Calsequestrin, a key protein in striated muscle health and disease.Journal of muscle research and cell motility · 2021Review
- The crosstalk between cardiomyocyte calcium and inflammasome signaling pathways in atrial fibrillation.Pflugers Archiv : European journal of physiology · 2021Review
- Simulating cardiac CaPflugers Archiv : European journal of physiology · 2021Article
- Excitation-contraction coupling and calcium release in atrial muscle.Pflugers Archiv : European journal of physiology · 2021Review
- Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Release of Ca(2+) from the sarcoplasmic reticulum (SR) drives contractile function of cardiac myocytes. Luminal Ca(2+) regulation of SR Ca(2+) release is fundamental not only in physiology but also in physiopathology because abnormal luminal Ca(2+) regulation is known to lead to arrhythmias, catecholaminergic polymorphic ventricular tachycardia (CPVT), and/or sudden cardiac arrest, as inferred from animal model studies. Luminal Ca(2+) regulates ryanodine receptor (RyR)2-mediated SR Ca(2+) release through mechanisms localized inside the SR; one of these involves luminal Ca(2+) interacting with calsequestrin (CASQ), triadin, and/or junctin to regulate RyR2 function. CASQ2-RyR2 regulation was examined at the single RyR2 channel level. Single RyR2s were incorporated into planar lipid bilayers by the fusion of native SR vesicles isolated from either wild-type (WT), CASQ2 knockout (KO), or R33Q-CASQ2 knock-in (KI) mice. KO and KI mice have CPVT-like phenotypes. We show that CASQ2(WT) action on RyR2 function (either activation or inhibition) was strongly influenced by the presence of cytosolic MgATP. Function of the reconstituted CASQ2(WT)-RyR2 complex was unaffected by changes in luminal free [Ca(2+)] (from 0.1 to 1 mM). The inhibition exerted by CASQ2(WT) association with the RyR2 determined a reduction in cytosolic Ca(2+) activation sensitivity. RyR2s from KO mice were significantly more sensitive to cytosolic Ca(2+) activation and had significantly longer mean open times than RyR2s from WT mice. Sensitivity of RyR2s from KI mice was in between that of RyR2 channels from KO and WT mice. Enhanced cytosolic RyR2 Ca(2+) sensitivity and longer RyR2 open times likely explain the CPVT-like phenotype of both KO and KI mice.
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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.