ArticleProceedings of the National Academy of Sciences of the United States of America1999
Tropomyosin directly modulates actomyosin mechanical performance at the level of a single actin filament.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- 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
- De Novo Asp219Val Mutation in Cardiac Tropomyosin Associated with Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Article
- Single-molecule imaging reveals the concerted release of myosin from regulated thin filaments.eLife · 2021Article
- Acidosis modifies effects of phosphorylated tropomyosin on the actin-myosin interaction in the myocardium.Journal of muscle research and cell motility · 2021Article
- Force Measurements From Myofibril to Filament.Frontiers in physiology · 2021Review
- Lysine acetylation of F-actin decreases tropomyosin-based inhibition of actomyosin activity.The Journal of biological chemistry · 2020Article
- Hypothesis: Single Actomyosin Properties Account for Ensemble Behavior in Active Muscle Shortening and Isometric Contraction.International journal of molecular sciences · 2020Article
- 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
- Distinct sites in tropomyosin specify shared and isoform-specific regulation of myosins II and V.Cytoskeleton (Hoboken, N.J.) · 2018Article
- Fission yeast myosin Myo2 is down-regulated in actin affinity by light chain phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cooperativity of myosin interaction with thin filaments is enhanced by stabilizing substitutions in tropomyosin.Journal of muscle research and cell motility · 2017Article
- Ca++-sensitizing mutations in troponin, P(i), and 2-deoxyATP alter the depressive effect of acidosis on regulated thin-filament velocity.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- A study of tropomyosin's role in cardiac function and disease using thin-filament reconstituted myocardium.Journal of muscle research and cell motility · 2013Review
- Regulation of actin-myosin interaction by conserved periodic sites of tropomyosin.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Filament compliance influences cooperative activation of thin filaments and the dynamics of force production in skeletal muscle.PLoS computational biology · 2012Article
- The role of tropomyosin domains in cooperative activation of the actin-myosin interaction.Journal of molecular biology · 2011Article
- Force spectroscopy reveals multiple "closed states" of the muscle thin filament.The Journal of biological chemistry · 2011Article
- Facilitated cross-bridge interactions with thin filaments by familial hypertrophic cardiomyopathy mutations in α-tropomyosin.Journal of biomedicine & biotechnology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Muscle contraction is the result of myosin cross-bridges (XBs) cyclically interacting with the actin-containing thin filament. This interaction is modulated by the thin filament regulatory proteins, troponin and tropomyosin (Tm). With the use of an in vitro motility assay, the role of Tm in myosin's ability to generate force and motion was assessed. At saturating myosin surface densities, Tm had no effect on thin filament velocity. However, below 50% myosin saturation, a significant reduction in actin-Tm filament velocity was observed, with complete inhibition of movement occurring at 12. 5% of saturating surface densities. Under similar conditions, actin filaments alone demonstrated no reduction in velocity. The effect of Tm on force generation was assessed at the level of a single thin filament. In the absence of Tm, isometric force was a linear function of the density of myosin on the motility surface. At 50% myosin surface saturation, the presence of Tm resulted in a 2-fold enhancement of force relative to actin alone. However, no further potentiation of force was observed with Tm at saturating myosin surface densities. These results indicate that, in the presence of Tm, the strong binding of myosin cooperatively activates the thin filament. The inhibition of velocity at low myosin densities and the potentiation of force at higher myosin densities suggest that Tm can directly modulate the kinetics of a single myosin XB and the recruitment of a population of XBs, respectively. At saturating myosin conditions, Tm does not appear to affect the recruitment or the kinetics of myosin XBs.
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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.