ArticleThe Journal of biological chemistry2010
Mechanism of regulation of native cardiac muscle thin filaments by rigor cardiac myosin-S1 and calcium.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Temperature dependence of activation of thick and thin filaments in skeletal and cardiac muscles.Journal of muscle research and cell motility · 2026Review
- Changing face of contractile activation in striated muscle at physiological temperature.The Journal of general physiology · 2023Article
- Myosin and tropomyosin-troponin complementarily regulate thermal activation of muscles.The Journal of general physiology · 2023Article
- Cooperativity of myosin II motors in the non-regulated and regulated thin filaments investigated with high-speed AFM.The Journal of general physiology · 2023Article
- Cryo-Electron Microscopy Reveals Cardiac Myosin Binding Protein-C M-Domain Interactions with the Thin Filament.Journal of molecular biology · 2022Article
- Cardiac myosin contraction and mechanotransduction in health and disease.The Journal of biological chemistry · 2021Review
- A troponin T variant linked with pediatric dilated cardiomyopathy reduces the coupling of thin filament activation to myosin and calcium binding.Molecular biology of the cell · 2021Article
- Troponin Revealed: Uncovering the Structure of the Thin Filament On-Off Switch in Striated Muscle.Biophysical journal · 2021Review
- Eliminating the First Inactive State and Stabilizing the Active State of the Cardiac Regulatory System Alters Behavior in Solution and in Ordered Systems.Biochemistry · 2020Article
- Cycling Cross-Bridges Contribute to Thin Filament Activation in Human Slow-Twitch Fibers.Frontiers in physiology · 2020Article
- Disrupted mechanobiology links the molecular and cellular phenotypes in familial dilated cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Computational Tool to Study Perturbations in Muscle Regulation and Its Application to Heart Disease.Biophysical journal · 2019Article
- Investigation into the mechanism of thin filament regulation by transient kinetics and equilibrium binding: Is there a conflict?The Journal of general physiology · 2019Review
- N-Terminal Domains of Cardiac Myosin Binding Protein C Cooperatively Activate the Thin Filament.Structure (London, England : 1993) · 2018Article
- Stepwise C-Terminal Truncation of Cardiac Troponin T Alters Function at Low and Saturating CaBiophysical journal · 2018Article
- CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Troponin C Mutations Partially Stabilize the Active State of Regulated Actin and Fully Stabilize the Active State When Paired with Δ14 TnT.Biochemistry · 2017Article
- Effect of N-Terminal Extension of Cardiac Troponin I on the Ca(2+) Regulation of ATP Binding and ADP Dissociation of Myosin II in Native Cardiac Myofibrils.Biochemistry · 2016Article
- Modulation of thin filament activation of myosin ATP hydrolysis by N-terminal domains of cardiac myosin binding protein-C.Biochemistry · 2014Article
- Three-dimensional organization of troponin on cardiac muscle thin filaments in the relaxed state.Biophysical journal · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
We have studied the mechanism of activation of native cardiac thin filaments by calcium and rigor myosin. The acceleration of the rate of 2'-deoxy-3'-O-(N-methylanthraniloyl)ADP (mdADP) dissociation from cardiac myosin-S1-mdADP-P(i) and cardiac myosin-S1-mdADP by native cardiac muscle thin filaments was measured using double mixing stopped-flow fluorescence. Relative to inhibited thin filaments (no bound calcium or rigor S1), fully activated thin filaments (with both calcium and rigor-S1 bound) increase the rate of product dissociation from the physiologically important pre-power stroke myosin-mdADP-P(i) by a factor of ∼75. This can be compared with only an ∼6-fold increase in the rate of nucleotide diphosphate dissociation from nonphysiological myosin-mdADP by the fully activated thin filaments relative to the fully inhibited thin filaments. These results show that physiological levels of regulation are not only dependent on the state of the thin filament but also on the conformation of the myosin. Less than 2-fold regulation is due to a change in affinity of myosin-ADP-P(i) for thin filaments such as would be expected by a simple "steric blocking" of the myosin-binding site of the thin filament by tropomyosin. Although maximal activation requires both calcium and rigor myosin-S1 bound to the cardiac filament, association with a single ligand produces ∼70% maximal activation. This can be contrasted with skeletal thin filaments in which calcium alone only activated the rate of product dissociation ∼20% of maximum, and rigor myosin produces ∼30% maximal activation.
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