ArticleBiophysical journal2017
Tropomyosin Must Interact Weakly with Actin to Effectively Regulate Thin Filament Function.
Article in Biophysical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Fine-tuning striated muscle performance: conserved sarcomere-level mechanisms across insect and vertebrate systems.Frontiers in physiology · 2026Review
- Dual role of Tropomyosin-R160 in thin filament regulation: Insights into phosphorylation-dependent cardiac relaxation and cardiomyopathy mechanisms.Archives of biochemistry and biophysics · 2025Article
- Article
- Duality in disease: How two amino acid substitutions at actin residue 312 result in opposing forms of cardiomyopathy.The Journal of biological chemistry · 2024Article
- Glutamate 139 of tropomyosin is critical for cardiac thin filament blocked-state stabilization.Journal of molecular and cellular cardiology · 2024Article
- Article
- Novel human cell expression method reveals the role and prevalence of posttranslational modification in nonmuscle tropomyosins.The Journal of biological chemistry · 2021Article
- Single-molecule imaging reveals the concerted release of myosin from regulated thin filaments.eLife · 2021Article
- M8R tropomyosin mutation disrupts actin binding and filament regulation: The beginning affects the middle and end.The Journal of biological chemistry · 2020Article
- Lysine acetylation of F-actin decreases tropomyosin-based inhibition of actomyosin activity.The Journal of biological chemistry · 2020Article
- Article
- The actin 'A-triad's' role in contractile regulation in health and disease.The Journal of physiology · 2020Review
- A role for actin flexibility in thin filament-mediated contractile regulation and myopathy.Nature communications · 2020Article
- Cardiomyopathy Mutation Alters End-to-End Junction of Tropomyosin and Reduces Calcium Sensitivity.Biophysical journal · 2020Article
- A Stochastic Multiscale Model of Cardiac Thin Filament Activation Using Brownian-Langevin Dynamics.Biophysical journal · 2019Article
- The Primary Causes of Muscle Dysfunction Associated with the Point Mutations in Tpm3.12; Conformational Analysis of Mutant Proteins as a Tool for Classification of Myopathies.International journal of molecular sciences · 2018Article
- Diabetes with heart failure increases methylglyoxal modifications in the sarcomere, which inhibit function.JCI insight · 2018Article
- The Molecular Mechanisms of Mutations in Actin and Myosin that Cause Inherited Myopathy.International journal of molecular sciences · 2018Review
- HCM and DCM cardiomyopathy-linked α-tropomyosin mutations influence off-state stability and crossbridge interaction on thin filaments.Archives of biochemistry and biophysics · 2018Article
- Tropomyosin isoforms differentially affect muscle contractility in the head and body regions of the nematode Caenorhabditis elegans.Molecular biology of the cell · 2018Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Elongated tropomyosin, associated with actin-subunits along the surface of thin filaments, makes electrostatic interactions with clusters of conserved residues, K326, K328, and R147, on actin. The association is weak, permitting low-energy cost regulatory movement of tropomyosin across the filament during muscle activation. Interestingly, acidic D292 on actin, also evolutionarily conserved, lies adjacent to the three-residue cluster of basic amino acids and thus may moderate the combined local positive charge, diminishing tropomyosin-actin interaction and facilitating regulatory-switching. Indeed, charge neutralization of D292 is connected to muscle hypotonia in individuals with D292V actin mutations and linked to congenital fiber-type disproportion. Here, the D292V mutation may predispose tropomyosin-actin positioning to a myosin-blocking state, aberrantly favoring muscle relaxation, thus mimicking the low-Ca
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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.