ArticlePloS one2013
Accelerated activation of SOCE current in myotubes from two mouse models of anesthetic- and heat-induced sudden death.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- ORAI1 inhibition as an efficient preclinical therapy for tubular aggregate myopathy and Stormorken syndrome.JCI insight · 2024Article
- Searching for Mechanisms Underlying the Assembly of Calcium Entry Units: The Role of Temperature and pH.International journal of molecular sciences · 2023Article
- Mutations in proteins involved in E-C coupling and SOCE and congenital myopathies.The Journal of general physiology · 2022Review
- Store-Operated CaInternational journal of molecular sciences · 2022Article
- Ablation of Calsequestrin-1, CaFrontiers in physiology · 2022Review
- Calsequestrin 1 Is an Active Partner of Stromal Interaction Molecule 2 in Skeletal Muscle.Cells · 2021Article
- A novel RyR1-selective inhibitor prevents and rescues sudden death in mouse models of malignant hyperthermia and heat stroke.Nature communications · 2021Article
- Altered CaMetabolites · 2021Review
- Calcium entry units (CEUs): perspectives in skeletal muscle function and disease.Journal of muscle research and cell motility · 2021Article
- Calsequestrin: a well-known but curious protein in skeletal muscle.Experimental & molecular medicine · 2020Review
- Pre-assembled Ca2+ entry units and constitutively active Ca2+ entry in skeletal muscle of calsequestrin-1 knockout mice.The Journal of general physiology · 2020Article
- 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
- Identification of drug modifiers for RYR1-related myopathy using a multi-species discovery pipeline.eLife · 2020Article
- Excessive Accumulation of CaFrontiers in physiology · 2019Article
- Role of STIM1/ORAI1-mediated store-operated CaCell calcium · 2018Review
- With the greatest care, stromal interaction molecule (STIM) proteins verify what skeletal muscle is doing.BMB reports · 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
- Article
- A focus on extracellular CaExperimental & molecular medicine · 2017Review
- Strenuous exercise triggers a life-threatening response in mice susceptible to malignant hyperthermia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
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 3 institutions in 2 countries.
Funding
Abstract
Store-operated calcium entry (SOCE) channels play an important role in Ca(2+) signaling. Recently, excessive SOCE was proposed to play a central role in the pathogenesis of malignant hyperthermia (MH), a pharmacogenic disorder of skeletal muscle. We tested this hypothesis by characterizing SOCE current (ISkCRAC) magnitude, voltage dependence, and rate of activation in myotubes derived from two mouse models of anesthetic- and heat-induced sudden death: 1) type 1 ryanodine receptor (RyR1) knock-in mice (Y524S/+) and 2) calsequestrin 1 and 2 double knock-out (dCasq-null) mice. ISkCRAC voltage dependence and magnitude at -80 mV were not significantly different in myotubes derived from wild type (WT), Y524S/+ and dCasq-null mice. However, the rate of ISkCRAC activation upon repetitive depolarization was significantly faster at room temperature in myotubes from Y524S/+ and dCasq-null mice. In addition, the maximum rate of ISkCRAC activation in dCasq-null myotubes was also faster than WT at more physiological temperatures (35-37°C). Azumolene (50 µM), a more water-soluble analog of dantrolene that is used to reverse MH crises, failed to alter ISkCRAC density or rate of activation. Together, these results indicate that while an increased rate of ISkCRAC activation is a common characteristic of myotubes derived from Y524S/+ and dCasq-null mice and that the protective effects of azumolene are not due to a direct inhibition of SOCE channels.
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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.