ReviewEuropean biophysics journal : EBJ2009
Ca(2+) signaling in striated muscle: the elusive roles of triadin, junctin, and calsequestrin.
Review in European biophysics journal : EBJ, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 50 citations in OpenAlex.
- Variants in ASPH cause exertional heat illness and are associated with malignant hyperthermia susceptibility.Nature communications · 2022Article
- Correlation of Phenotype-Genotype and Protein Structure inFrontiers in neurology · 2022Article
- Pathological mechanisms of vacuolar aggregate myopathy arising from a Casq1 mutation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Motor Unit Force Potentiation and Calcium Handling Protein Concentration in Rat Fast Muscle After Resistance Training.Frontiers in physiology · 2021Article
- Structure of RyR1 in native membranes.EMBO reports · 2020Article
- CaCells · 2019Review
- Calcium Mechanisms in Limb-Girdle Muscular Dystrophy withInternational journal of molecular sciences · 2019Review
- Two pools of IRE1α in cardiac and skeletal muscle cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Article
- Muscle-specific regulation of right ventricular transcriptional responses to chronic hypoxia-induced hypertrophy by the muscle ring finger-1 (MuRF1) ubiquitin ligase in mice.BMC medical genetics · 2018Article
- Review of RyR1 pathway and associated pathomechanisms.Acta neuropathologica communications · 2016Review
- Calsequestrin interacts directly with the cardiac ryanodine receptor luminal domain.Journal of cell science · 2016Article
- Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease.Frontiers in physiology · 2015Review
- Altered expression and splicing of Ca(2+) metabolism genes in myotonic dystrophies DM1 and DM2.Neuropathology and applied neurobiology · 2013Article
- Skeletal muscle fibers: Inactivated or depleted after long depolarizations?The Journal of general physiology · 2013Article
- Ryanodine receptors: structure and function.The Journal of biological chemistry · 2012Review
- Dietary nitrate increases tetanic [Ca2+]i and contractile force in mouse fast-twitch muscle.The Journal of physiology · 2012Article
- Role of Junctin protein interactions in cellular dynamics of calsequestrin polymer upon calcium perturbation.The Journal of biological chemistry · 2012Article
- Reciprocal dihydropyridine and ryanodine receptor interactions in skeletal muscle activation.Journal of muscle research and cell motility · 2011Review
- Differential effect of calsequestrin ablation on structure and function of fast and slow skeletal muscle fibers.Journal of biomedicine & biotechnology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review focuses on molecular interactions between calsequestrin, triadin, junctin and the ryanodine receptor in the lumen of the sarcoplasmic reticulum. These interactions modulate changes in Ca(2+) release in response to changes in the Ca(2+) load within the sarcoplasmic reticulum store in striated muscle and are of fundamental importance to Ca(2+) homeostasis, since massive adaptive changes occur when expression of the proteins is manipulated, while mutations in calsequestrin lead to functional changes which can be fatal. We find that calsequestrin plays a different role in the heart and skeletal muscle, enhancing Ca(2+) release in the heart, but depressing Ca(2+) release in skeletal muscle. We also find that triadin and junctin exert independent influences on the ryanodine receptor in skeletal muscle where triadin alone modifies excitation-contraction coupling, while junctin alone supports functional interactions between calsequestrin and the ryanodine receptor.
Indexed as
Identifiers
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.