ArticleJournal of muscle research and cell motility1998
A strain-dependent ratchet model for [phosphate]- and [ATP]-dependent muscle contraction.
Article in Journal of muscle research and cell motility, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Advancing clinical translation of cardiac biomechanics models: a comprehensive review, applications and future pathways.Frontiers in physics · 2023Article
- Mechanisms of Frank-Starling law of the heart and stretch activation in striated muscles may have a common molecular origin.Journal of muscle research and cell motility · 2021Article
- A cross-bridge cycle with two tension-generating steps simulates skeletal muscle mechanics.Biophysical journal · 2013Article
- Interventricular comparison of the energetics of contraction of trabeculae carneae isolated from the rat heart.The Journal of physiology · 2013Article
- Force transients and minimum cross-bridge models in muscular contraction.Journal of muscle research and cell motility · 2007Review
- Multi-scale modelling and the IUPS physiome project.Journal of molecular histology · 2004Article
- Mechanokinetics of rapid tension recovery in muscle: the Myosin working stroke is followed by a slower release of phosphate.Biophysical journal · 2004Article
- Protein-protein ratchets: stochastic simulation and application to processive enzymes.Biophysical journal · 2001Article
- Direct tests of muscle cross-bridge theories: predictions of a Brownian dumbbell model for position-dependent cross-bridge lifetimes and step sizes with an optically trapped actin filament.Biophysical journal · 1998Article
- Comments on the paper by Dr. David Smith entitled "A strain-dependent ratchet model for [phosphate]- and [ATP]-dependent muscle contraction".Journal of muscle research and cell motility · 1998Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
A minimal strain-dependent ratchet model of muscle cross-bridge action is proposed which is broadly compatible with structural and kinetic constraints. Its essential features are: (1) dynamic binding of the S1-products complex to actin through a disorder-order transition coupled to the release of inorganic phosphate; (2) the absence of a force-generating rotation of the myosin head between the two force-holding states A.M.ADP and A.M; (3) strain-control of ADP release and ATP binding, giving net isometric tension and directed motility by the selective dissociation of negatively strained bound states. With a disordered pre-force state, the binding rate to state A.M.ADP need not be symmetric in x, the actin site displacement. With faster binding at positive x, the model predicts many steady-state and transient properties of striated muscle observed experimentally, including phases 2-4 of tension recovery from length changes and their dependence on excess phosphate (which enhances and accelerates phase 3) and reduced ATP (which gives a bimodal phase 2 and slows one mode). The response to large perturbations is often sensitive to the number of actin sites used, and to the inclusion of a 1 nm displacement of the neck region on release of ADP. The latter stabilizes the periodic tension behaviour produced by repeated releases.
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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.