ArticleThe Journal of biological chemistry2014
Magnesium modulates actin binding and ADP release in myosin motors.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Impact of salt concentration and free magnesium on human beta-cardiac myosin reveal important details about the conserved mechanochemical mechanism.The Journal of biological chemistry · 2026Article
- On the Control of Directionality of Myosin.Journal of the American Chemical Society · 2024Article
- Dilated cardiomyopathy mutation in beta-cardiac myosin enhances actin activation of the power stroke and phosphate release.PNAS nexus · 2024Article
- Conformational changes linked to ADP release from human cardiac myosin bound to actin-tropomyosin.The Journal of general physiology · 2023Article
- Changes in the urinary proteome of rats after short-term intake of magnesium L-threonate(MgT).Frontiers in nutrition · 2023Article
- Directionality of PYD filament growth determined by the transition of NLRP3 nucleation seeds to ASC elongation.Science advances · 2022Article
- Divalent magnesium restores cytoskeletal storage lesions in cold-stored platelet concentrates.Scientific reports · 2022Article
- Switch-1 instability at the active site decouples ATP hydrolysis from force generation in myosin II.Cytoskeleton (Hoboken, N.J.) · 2021Article
- FRET and optical trapping reveal mechanisms of actin activation of the power stroke and phosphate release in myosin V.The Journal of biological chemistry · 2020Article
- Structural and Computational Insights into a Blebbistatin-Bound Myosin•ADP Complex with Characteristics of an ADP-Release Conformation along the Two-Step Myosin Power Stoke.International journal of molecular sciences · 2020Article
- Unconventional Myosins: How Regulation Meets Function.International journal of molecular sciences · 2019Review
- Dilated cardiomyopathy mutation in the converter domain of human cardiac myosin alters motor activity and response to omecamtiv mecarbil.The Journal of biological chemistry · 2019Article
- Interplay of actin, ADP and MgArchives of biochemistry and biophysics · 2019Article
- Converter domain mutations in myosin alter structural kinetics and motor function.The Journal of biological chemistry · 2019Article
- Nanothermometry Reveals Calcium-Induced Remodeling of Myosin.Nano letters · 2018Article
- Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular CaCold Spring Harbor perspectives in medicine · 2018Review
- Modeling the Actin.myosin ATPase Cross-Bridge Cycle for Skeletal and Cardiac Muscle Myosin Isoforms.Biophysical journal · 2017Article
- Defects in TRPM7 channel function deregulate thrombopoiesis through altered cellular Mg(2+) homeostasis and cytoskeletal architecture.Nature communications · 2016Article
- Modulating Beta-Cardiac Myosin Function at the Molecular and Tissue Levels.Frontiers in physiology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
We examined the magnesium dependence of five class II myosins, including fast skeletal muscle myosin, smooth muscle myosin, β-cardiac myosin (CMIIB), Dictyostelium myosin II (DdMII), and nonmuscle myosin IIA, as well as myosin V. We found that the myosins examined are inhibited in a Mg(2+)-dependent manner (0.3-9.0 mm free Mg(2+)) in both ATPase and motility assays, under conditions in which the ionic strength was held constant. We found that the ADP release rate constant is reduced by Mg(2+) in myosin V, smooth muscle myosin, nonmuscle myosin IIA, CMIIB, and DdMII, although the ADP affinity is fairly insensitive to Mg(2+) in fast skeletal muscle myosin, CMIIB, and DdMII. Single tryptophan probes in the switch I (Trp-239) and switch II (Trp-501) region of DdMII demonstrate these conserved regions of the active site are sensitive to Mg(2+) coordination. Cardiac muscle fiber mechanic studies demonstrate cross-bridge attachment time is increased at higher Mg(2+) concentrations, demonstrating that the ADP release rate constant is slowed by Mg(2+) in the context of an activated muscle fiber. Direct measurements of phosphate release in myosin V demonstrate that Mg(2+) reduces actin affinity in the M·ADP·Pi state, although it does not change the rate of phosphate release. Therefore, the Mg(2+) inhibition of the actin-activated ATPase activity observed in class II myosins is likely the result of Mg(2+)-dependent alterations in actin binding. Overall, our results suggest that Mg(2+) reduces the ADP release rate constant and rate of attachment to actin in both high and low duty ratio myosins.
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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.