ReviewThe Journal of physiology2009
Junctin and the histidine-rich Ca2+ binding protein: potential roles in heart failure and arrhythmogenesis.
Review in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes.JACC. Basic to translational science · 2026Article
- Determinants of Ca2+ release restitution: Insights from genetically altered animals and mathematical modeling.The Journal of general physiology · 2020Article
- The Histidine-Rich Calcium Binding Protein in Regulation of Cardiac Rhythmicity.Frontiers in physiology · 2018Review
- The role of luminal Ca regulation in Ca signaling refractoriness and cardiac arrhythmogenesis.The Journal of general physiology · 2017Review
- Exploration of haplotype research consortium imputation for genome-wide association studies in 20,032 Generation Scotland participants.Genome medicine · 2017Article
- Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVT.Cardiovascular research · 2015Article
- Malignant hyperthermia: a review.Orphanet journal of rare diseases · 2015Review
- The couplonopathies: A comparative approach to a class of diseases of skeletal and cardiac muscle.The Journal of general physiology · 2015Review
- Loss of muscleblind-like 1 results in cardiac pathology and persistence of embryonic splice isoforms.Scientific reports · 2015Article
- Signaling in muscle contraction.Cold Spring Harbor perspectives in biology · 2015Review
- Ca handling during excitation-contraction coupling in heart failure.Pflugers Archiv : European journal of physiology · 2014Review
- Store-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling.Journal of molecular and cellular cardiology · 2013Review
- An altered expression of genes involved in the regulation of ion channels in atrial myocytes is correlated with the risk of atrial fibrillation in patients with heart failure.Experimental and therapeutic medicine · 2013Article
- Altered sarcoplasmic reticulum calcium cycling--targets for heart failure therapy.Nature reviews. Cardiology · 2012Review
- Role of Junctin protein interactions in cellular dynamics of calsequestrin polymer upon calcium perturbation.The Journal of biological chemistry · 2012Article
- Dual role of junctin in the regulation of ryanodine receptors and calcium release in cardiac ventricular myocytes.The Journal of physiology · 2011Article
- The Ca2+ pumps of the endoplasmic reticulum and Golgi apparatus.Cold Spring Harbor perspectives in biology · 2011Review
- Organellar calcium buffers.Cold Spring Harbor perspectives in biology · 2011Review
- Silencing genes of sarcoplasmic reticulum proteins clarifies their roles in excitation-contraction coupling.The Journal of physiology · 2009Article
- Junctin - the quiet achiever.The Journal of physiology · 2009Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Contractile dysfunction and ventricular arrhythmias associated with heart failure have been attributed to aberrant sarcoplasmic reticulum (SR) Ca(2+) cycling. The study of junctin (JCN) and histidine-rich Ca(2+) binding protein (HRC) becomes of particular importance since these proteins have been shown to be critical regulators of Ca(2+) cycling. Specifically, JCN is a SR membrane protein, which is part of the SR Ca(2+) release quaternary structure that also includes the ryanodine receptor, triadin and calsequestrin. Functionally, JCN serves as a bridge between calsequestrin and the Ca(2+) release channel, ryanodine receptor. HRC is a SR luminal Ca(2+) binding protein known to associate with both triadin and the sarcoplasmic reticulum Ca(2+)-ATPase, and may thus mediate the crosstalk between SR Ca(2+) uptake and release. Indeed, evidence from genetic models of JCN and HRC indicate that they are important in cardiophysiology as alterations in these proteins affect SR Ca(2+) handling and cardiac function. In addition, downregulation of JCN and HRC may contribute to Ca(2+) cycling perturbations manifest in the failing heart, where their protein levels are significantly reduced. This review examines the roles of JCN and HRC in SR Ca(2+) cycling and their potential significance in heart failure.
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What OpenQuestion holds
Registered trials
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.