ArticlePLoS computational biology2007
Sarcomere lattice geometry influences cooperative myosin binding in muscle.
Article in PLoS computational biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 108 citations in OpenAlex.
- Cross-bridge model for predicting muscle short-range stiffness during movement.PLoS computational biology · 2026Article
- Isometric slow- and fast-contracting skeletal muscle fibres have more similar cellular and molecular properties at 37°C than at 25°C in older adults.The Journal of physiology · 2026Article
- The E525K β-Myosin Mutation Causes Hypocontractility in Cardiomyocytes Without Altering Loaded Crossbridge Cycling.bioRxiv : the preprint server for biology · 2026Article
- Nanometer scale difference in myofilament lattice structure of muscle alters muscle function in a spatially explicit model.PLoS computational biology · 2025Article
- Modeling cardiac contractile cooperativity across species.The Journal of general physiology · 2025Article
- Modeling the effects of thin filament near-neighbor cooperative interactions in mammalian myocardium.The Journal of general physiology · 2025Article
- Bayesian estimation of muscle mechanisms and therapeutic targets using variational autoencoders.Biophysical journal · 2025Article
- Bayesian Estimation of Muscle Mechanisms and Therapeutic Targets Using Variational Autoencoders.bioRxiv : the preprint server for biology · 2024Article
- Article
- A novel kinetic model to demonstrate the independent effects of ATP and ADP/Pi concentrations on sarcomere function.PLoS computational biology · 2024Article
- Modeling thick filament activation suggests a molecular basis for force depression.Biophysical journal · 2024Article
- Design Principles and Benefits of Spatially Explicit Models of Myofilament Function.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023Review
- Basic science methods for the characterization of variants of uncertain significance in hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- Mitochondrial network configuration influences sarcomere and myosin filament structure in striated muscles.Nature communications · 2022Article
- FiberSim: A flexible open-source model of myofilament-level contraction.Biophysical journal · 2022Article
- Hypertrophic cardiomyopathy β-cardiac myosin mutation (P710R) leads to hypercontractility by disrupting super relaxed state.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Force-velocity and tension transient measurements from Drosophila jump muscle reveal the necessity of both weakly-bound cross-bridges and series elasticity in models of muscle contraction.Archives of biochemistry and biophysics · 2021Article
- The effects of inorganic phosphate on muscle force development and energetics: challenges in modelling related to experimental uncertainties.Journal of muscle research and cell motility · 2021Article
- Multiscale modeling of twitch contractions in cardiac trabeculae.The Journal of general physiology · 2021Article
5 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
In muscle, force emerges from myosin binding with actin (forming a cross-bridge). This actomyosin binding depends upon myofilament geometry, kinetics of thin-filament Ca(2+) activation, and kinetics of cross-bridge cycling. Binding occurs within a compliant network of protein filaments where there is mechanical coupling between myosins along the thick-filament backbone and between actin monomers along the thin filament. Such mechanical coupling precludes using ordinary differential equation models when examining the effects of lattice geometry, kinetics, or compliance on force production. This study uses two stochastically driven, spatially explicit models to predict levels of cross-bridge binding, force, thin-filament Ca(2+) activation, and ATP utilization. One model incorporates the 2-to-1 ratio of thin to thick filaments of vertebrate striated muscle (multi-filament model), while the other comprises only one thick and one thin filament (two-filament model). Simulations comparing these models show that the multi-filament predictions of force, fractional cross-bridge binding, and cross-bridge turnover are more consistent with published experimental values. Furthermore, the values predicted by the multi-filament model are greater than those values predicted by the two-filament model. These increases are larger than the relative increase of potential inter-filament interactions in the multi-filament model versus the two-filament model. This amplification of coordinated cross-bridge binding and cycling indicates a mechanism of cooperativity that depends on sarcomere lattice geometry, specifically the ratio and arrangement of myofilaments.
Indexed as
Identifiers
What OpenQuestion holds
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.