ArticleJournal of molecular biology2008
Structural basis for the regulation of muscle contraction by troponin and tropomyosin.
Article in Journal of molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 212 citations in OpenAlex.
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- Arg92Leu-cTnT Alters the cTnC-cTnI Interface Disrupting PKA-Mediated Relaxation.Circulation research · 2024Article
- From amino-acid to disease: the effects of oxidation on actin-myosin interactions in muscle.Journal of muscle research and cell motility · 2023Review
- Troponin-I-induced tropomyosin pivoting defines thin-filament function in relaxed and active muscle.The Journal of general physiology · 2023Article
- Urine High-Sensitive Troponin T-Novel Biomarker of Myocardial Damage in Children.Reviews in cardiovascular medicine · 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
- Effects of thermal acclimation on the proteome of the planarian Crenobia alpina from an alpine freshwater spring.The Journal of experimental biology · 2022Article
- Structure and Dynamics of the Flexible Cardiac Troponin T Linker Domain in a Fully Reconstituted Thin Filament.Biochemistry · 2022Article
- Review
- Small Angle X-ray Diffraction as a Tool for Structural Characterization of Muscle Disease.International journal of molecular sciences · 2022Review
- Transcriptomic Analysis of Fish Hosts Responses to Nervous Necrosis Virus.Pathogens (Basel, Switzerland) · 2022Review
- Validate the force-velocity relation of the Hill's muscle model from a molecular perspective.Frontiers in bioengineering and biotechnology · 2022Article
- Significance of Cardiac Troponins as an Identification Tool in COVID-19 Patients Using Biosensors: An Update.Frontiers in molecular biosciences · 2022Review
- Cardiomyocyte Dysfunction in Inherited Cardiomyopathies.International journal of molecular sciences · 2021Review
- Single-molecule imaging reveals the concerted release of myosin from regulated thin filaments.eLife · 2021Article
- CaOxidative medicine and cellular longevity · 2021Article
- Sarcomeric myopathies associated with tremor: new insights and perspectives.Journal of muscle research and cell motility · 2020Article
- Mechanical contribution to muscle thin filament activation.The Journal of biological chemistry · 2020Article
- Actin-binding compounds, previously discovered by FRET-based high-throughput screening, differentially affect skeletal and cardiac muscle.The Journal of biological chemistry · 2020Article
36 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The molecular switching mechanism governing skeletal and cardiac muscle contraction couples the binding of Ca2+ on troponin to the movement of tropomyosin on actin filaments. Despite years of investigation, this mechanism remains unclear because it has not yet been possible to directly assess the structural influence of troponin on tropomyosin that causes actin filaments, and hence myosin-crossbridge cycling and contraction, to switch on and off. A C-terminal domain of troponin I is thought to be intimately involved in inducing tropomyosin movement to an inhibitory position that blocks myosin-crossbridge interaction. Release of this regulatory, latching domain from actin after Ca2+ binding to TnC (the Ca2+ sensor of troponin that relieves inhibition) presumably allows tropomyosin movement away from the inhibitory position on actin, thus initiating contraction. However, the structural interactions of the regulatory domain of TnI (the "inhibitory" subunit of troponin) with tropomyosin and actin that cause tropomyosin movement are unknown, and thus, the regulatory process is not well defined. Here, thin filaments were labeled with an engineered construct representing C-terminal TnI, and then, 3D electron microscopy was used to resolve where troponin is anchored on actin-tropomyosin. Electron microscopy reconstruction showed how TnI binding to both actin and tropomyosin at low Ca2+ competes with tropomyosin for a common site on actin and drives tropomyosin movement to a constrained, relaxing position to inhibit myosin-crossbridge association. Thus, the observations reported reveal the structural mechanism responsible for troponin-tropomyosin-mediated steric interference of actin-myosin interaction that regulates muscle contraction.
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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.