ArticleBiophysical journal2012
Temperature and RyR1 regulate the activation rate of store-operated Ca²+ entry current in myotubes.
Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Structural rearrangements underlying the activation of STIM1 by ER calcium depletion.bioRxiv : the preprint server for biology · 2026Article
- Searching for Mechanisms Underlying the Assembly of Calcium Entry Units: The Role of Temperature and pH.International journal of molecular sciences · 2023Article
- Acute exposure to extracellular BTP2 does not inhibit Ca2+ release during EC coupling in intact skeletal muscle fibers.The Journal of general physiology · 2022Article
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Review
- Calcium entry units (CEUs): perspectives in skeletal muscle function and disease.Journal of muscle research and cell motility · 2021Article
- Preclinical model systems of ryanodine receptor 1-related myopathies and malignant hyperthermia: a comprehensive scoping review of works published 1990-2019.Orphanet journal of rare diseases · 2020Article
- TRPCs: Influential Mediators in Skeletal Muscle.Cells · 2020Review
- VIP and muscarinic synergistic mucin secretion by salivary mucous cells is mediated by enhanced PKC activity via VIP-induced release of an intracellular CaPflugers Archiv : European journal of physiology · 2020Article
- Temperature-dependent increase in the calcium sensitivity and acceleration of activation of ANO6 chloride channel variants.Scientific reports · 2019Article
- Role of STIM1/ORAI1-mediated store-operated CaCell calcium · 2018Review
- The Complex Role of Store Operated Calcium Entry Pathways and Related Proteins in the Function of Cardiac, Skeletal and Vascular Smooth Muscle Cells.Frontiers in physiology · 2018Review
- Functional impact of an oculopharyngeal muscular dystrophy mutation in PABPN1.The Journal of physiology · 2017Article
- Axonal Endoplasmic Reticulum CaNeuron · 2017Article
- Orai1 enhances muscle endurance by promoting fatigue-resistant type I fiber content but not through acute store-operated Ca2+ entry.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Role of the JP45-Calsequestrin Complex on Calcium Entry in Slow Twitch Skeletal Muscles.The Journal of biological chemistry · 2016Article
- A quantitative description of tubular system Ca(2+) handling in fast- and slow-twitch muscle fibres.The Journal of physiology · 2016Article
- Malignant hyperthermia: a review.Orphanet journal of rare diseases · 2015Review
- Enhanced Ca²⁺ influx from STIM1-Orai1 induces muscle pathology in mouse models of muscular dystrophy.Human molecular genetics · 2014Article
- The ryanodine receptor agonist 4-chloro-3-ethylphenol blocks ORAI store-operated channels.British journal of pharmacology · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Store-operated calcium entry (SOCE) is an important Ca(2+) entry pathway in skeletal muscle. However, direct electrophysiological recording and full characterization of the underlying SOCE current in skeletal muscle cells (I(SkCRAC)) has not been reported. Here, we characterized the biophysical properties, pharmacological profile, and molecular identity of I(SkCRAC) in skeletal myotubes, as well as the regulation of its rate of activation by temperature and the type I ryanodine receptor (RyR1). I(SkCRAC) exhibited many hallmarks of Ca(2+) release activated Ca(2+) currents (I(CRAC)): store dependence, strong inward rectification, positive reversal potential, limited cesium permeability, and sensitivity to SOCE channel blockers. I(SkCRAC) was reduced by siRNA knockdown of stromal interaction molecule 1 and expression of dominant negative Orai1. Average I(SkCRAC) current density at -80mV was 1.00 ± 0.05 pA/pF. In the presence of 20 mM intracellular EGTA, I(SkCRAC) activation occurred over tens of seconds during repetitive depolarization at 0.5Hz and was inhibited by treatment with 100 μM ryanodine. The rate of SOCE activation was reduced threefold in myotubes from RyR1-null mice and increased 4.6-fold at physiological temperatures (35-37°C). These results show that I(SkCRAC) exhibits similar biophysical, pharmacological, and molecular properties as I(CRAC) in nonexcitable cells and its rate of activation during repetitive depolarization is strongly regulated by temperature and RyR1 activity.
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