ArticleBiophysical journal2006
Transient loss of voltage control of Ca2+ release in the presence of maurocalcine in skeletal muscle.
Article in Biophysical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Probenecid affects muscle Ca2+ homeostasis and contraction independently from pannexin channel block.The Journal of general physiology · 2023Article
- Superfast excitation-contraction coupling in adult zebrafish skeletal muscle fibers.The Journal of general physiology · 2022Article
- Impaired excitation-contraction coupling in muscle fibres from the dynamin2The Journal of physiology · 2017Article
- Phosphatidylinositol 3-kinase inhibition restores Ca2+ release defects and prolongs survival in myotubularin-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Maurocalcin phosphorylated at threonin 26 maintains its activity on ryanodine receptor-mediated Ca2+ release in intact muscle fibers.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- In cellulo phosphorylation induces pharmacological reprogramming of maurocalcin, a cell-penetrating venom peptide.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Depression of voltage-activated Ca2+ release in skeletal muscle by activation of a voltage-sensing phosphatase.The Journal of general physiology · 2015Article
- Phosphoinositide substrates of myotubularin affect voltage-activated Ca²⁺ release in skeletal muscle.Pflugers Archiv : European journal of physiology · 2014Article
- Ca2+ release in muscle fibers expressing R4892W and G4896V type 1 ryanodine receptor disease mutants.PloS one · 2013Article
- Small efficient cell-penetrating peptides derived from scorpion toxin maurocalcine.The Journal of biological chemistry · 2012Article
- Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control.The Journal of general physiology · 2012Article
- Junctophilin 1 and 2 proteins interact with the L-type Ca2+ channel dihydropyridine receptors (DHPRs) in skeletal muscle.The Journal of biological chemistry · 2011Article
- Defects in Ca2+ release associated with local expression of pathological ryanodine receptors in mouse muscle fibres.The Journal of physiology · 2011Article
- Model calcium sensors for network homeostasis: sensor and readout parameter analysis from a database of model neuronal networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Design of a disulfide-less, pharmacologically inert, and chemically competent analog of maurocalcine for the efficient transport of impermeant compounds into cells.The Journal of biological chemistry · 2008Article
- Charged surface area of maurocalcine determines its interaction with the skeletal ryanodine receptor.Biophysical journal · 2008Article
- Spontaneous and voltage-activated Ca2+ release in adult mouse skeletal muscle fibres expressing the type 3 ryanodine receptor.The Journal of physiology · 2008Article
- Maurocalcine interacts with the cardiac ryanodine receptor without inducing channel modification.The Biochemical journal · 2007Article
- The elusive role of the SPRY2 domain in RyR1.Channels (Austin, Tex.)Article
- Voltage-activated elementary calcium release events in isolated mouse skeletal muscle fibers.The Journal of membrane biologyArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In skeletal muscle, sarcoplasmic reticulum (SR) calcium release is controlled by the plasma membrane voltage through interactions between the voltage-sensing dihydropyridine receptor (DHPr) and the ryanodine receptor (RYr) calcium release channel. Maurocalcine (MCa), a scorpion toxin peptide presenting some homology with a segment of a cytoplasmic loop of the DHPr, has been previously shown to strongly affect the activity of the isolated RYr. We injected MCa into mouse skeletal muscle fibers and measured intracellular calcium under voltage-clamp conditions. Voltage-activated calcium transients exhibited similar properties in control and in MCa-injected fibers during the depolarizing pulses, and the voltage dependence of calcium release was similar under the two conditions. However, MCa was responsible for a pronounced sustained phase of Ca(2+) elevation that proceeded for seconds following membrane repolarization, with no concurrent alteration of the membrane current. The magnitude of the underlying uncontrolled extra phase of Ca(2+) release correlated well with the peak calcium release during the pulse. Results suggest that MCa binds to RYr that open on membrane depolarization and that this interaction specifically alters the process of repolarization-induced closure of the channels.
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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.