ArticleThe Journal of biological chemistry2013
Type 1 inositol (1,4,5)-trisphosphate receptor activates ryanodine receptor 1 to mediate calcium spark signaling in adult mammalian skeletal muscle.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- Remodeling of the ryanodine receptor isoform 1 channel regulates the sweet and umami taste perception ofFundamental research · 2023Article
- Skeletal Ryanodine Receptors Are Involved in Impaired Myogenic Differentiation in Duchenne Muscular Dystrophy Patients.International journal of molecular sciences · 2021Article
- TRIC-A regulates intracellular CaPflugers Archiv : European journal of physiology · 2021Review
- Diabetes mellitus exacerbates post-myocardial infarction heart failure by reducing sarcolipin promoter methylation.ESC heart failure · 2020Article
- Article
- TRIC-A Channel Maintains Store Calcium Handling by Interacting With Type 2 Ryanodine Receptor in Cardiac Muscle.Circulation research · 2020Article
- PDK4 Augments ER-Mitochondria Contact to Dampen Skeletal Muscle Insulin Signaling During Obesity.Diabetes · 2019Article
- Intracellular Calcium Mobilization Is Required for Sonic Hedgehog Signaling.Developmental cell · 2018Article
- Mitochondrial Calcium Increase Induced by RyR1 and IP3R Channel Activation After Membrane Depolarization Regulates Skeletal Muscle Metabolism.Frontiers in physiology · 2018Article
- Proteolytic fragmentation of inositol 1,4,5-trisphosphate receptors: a novel mechanism regulating channel activity?The Journal of physiology · 2016Review
- Phosphoinositides in Ca(2+) signaling and excitation-contraction coupling in skeletal muscle: an old player and newcomers.Journal of muscle research and cell motility · 2015Review
- Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy.Cell death and differentiation · 2015Review
- Depression of voltage-activated Ca2+ release in skeletal muscle by activation of a voltage-sensing phosphatase.The Journal of general physiology · 2015Article
- Lysosomal two-pore channel subtype 2 (TPC2) regulates skeletal muscle autophagic signaling.The Journal of biological chemistry · 2015Article
- Localized nuclear and perinuclear Ca(2+) signals in intact mouse skeletal muscle fibers.Frontiers in physiology · 2015Article
- Monovalent cationic channel activity in the inner membrane of nuclei from skeletal muscle fibers.Biophysical journal · 2014Article
- Intracellular calcium channels in protozoa.European journal of pharmacology · 2014Review
- Calcium release from intra-axonal endoplasmic reticulum leads to axon degeneration through mitochondrial dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Assessment of calcium sparks in intact skeletal muscle fibers.Journal of visualized experiments : JoVE · 2014Article
- Trimeric intracellular cation channels and sarcoplasmic/endoplasmic reticulum calcium homeostasis.Circulation research · 2014Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Functional coupling between inositol (1,4,5)-trisphosphate receptor (IP(3)R) and ryanodine receptor (RyR) represents a critical component of intracellular Ca(2+) signaling in many excitable cells; however, the role of this mechanism in skeletal muscle remains elusive. In skeletal muscle, RyR-mediated Ca(2+) sparks are suppressed in resting conditions, whereas application of transient osmotic stress can trigger activation of Ca(2+) sparks that are restricted to the periphery of the fiber. Here we show that onset of these spatially confined Ca(2+) sparks involves interaction between activation of IP(3)R and RyR near the sarcolemmal membrane. Pharmacological prevention of IP(3) production or inhibition of IP(3)R channel activity abolishes stress-induced Ca(2+) sparks in skeletal muscle. Although genetic ablation of the type 2 IP(3)R does not appear to affect Ca(2+) sparks in skeletal muscle, specific silencing of the type 1 IP(3)R leads to ablation of stress-induced Ca(2+) sparks. Our data indicate that membrane-delimited signaling involving cross-talk between IP(3)R1 and RyR1 contributes to Ca(2+) spark activation in skeletal muscle.
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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.