ArticleBiophysical journal1999
Regulation of skeletal muscle tension redevelopment by troponin C constructs with different Ca2+ affinities.
Article in Biophysical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Cardiac Troponin C E135A Variant Impairs Myofilament Response to PKA Phosphorylation and Is Associated With Autosomal Dominant Dilated Cardiomyopathy With Diastolic Dysfunction.Circulation. Genomic and precision medicine · 2025Article
- Cardiac troponin T N-domain variant destabilizes the actin interface resulting in disturbed myofilament function.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Mandibular muscle troponin of the Florida carpenter ant Camponotus floridanus: extending our insights into invertebrate CaJournal of muscle research and cell motility · 2021Article
- Anomalous structural dynamics of minimally frustrated residues in cardiac troponin C triggers hypertrophic cardiomyopathy.Chemical science · 2021Article
- The intrinsically disordered C terminus of troponin T binds to troponin C to modulate myocardial force generation.The Journal of biological chemistry · 2019Article
- A Dynamic Situation with Uncertainty: Multiscale Modeling of Cardiac Thin-Filament CaBiophysical journal · 2019Article
- Familial Dilated Cardiomyopathy Associated With a Novel Combination of Compound HeterozygousFrontiers in physiology · 2019Article
- Structural and functional impact of troponin C-mediated CaJournal of molecular and cellular cardiology · 2018Article
- Structural determinants of muscle thin filament cooperativity.Archives of biochemistry and biophysics · 2016Review
- AAV6-mediated Cardiac-specific Overexpression of Ribonucleotide Reductase Enhances Myocardial Contractility.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Fluorescent Protein-Based Ca2+ Sensor Reveals Global, Divalent Cation-Dependent Conformational Changes in Cardiac Troponin C.PloS one · 2016Article
- The embryonic myosin R672C mutation that underlies Freeman-Sheldon syndrome impairs cross-bridge detachment and cycling in adult skeletal muscle.Human molecular genetics · 2015Article
- Slowed Dynamics of Thin Filament Regulatory Units Reduces CaCellular and molecular bioengineering · 2013Article
- Tropomyosin flexural rigidity and single ca(2+) regulatory unit dynamics: implications for cooperative regulation of cardiac muscle contraction and cardiomyocyte hypertrophy.Frontiers in physiology · 2012Article
- Effect of Ca2+ binding properties of troponin C on rate of skeletal muscle force redevelopment.American journal of physiology. Cell physiology · 2010Article
- Length dependence of force generation exhibit similarities between rat cardiac myocytes and skeletal muscle fibres.The Journal of physiology · 2010Article
- Modulation of troponin C affinity for the thin filament by different cross-bridge states in skinned skeletal muscle fibers.Pflugers Archiv : European journal of physiology · 2008Article
- Thin filament Ca2+ binding properties and regulatory unit interactions alter kinetics of tension development and relaxation in rabbit skeletal muscle.The Journal of physiology · 2008Article
- Influence of enhanced troponin C Ca2+-binding affinity on cooperative thin filament activation in rabbit skeletal muscle.The Journal of physiology · 2007Article
- Toward protein structure in situ: comparison of two bifunctional rhodamine adducts of troponin C.Biophysical journal · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
In maximally activated skinned fibers, the rate of tension redevelopment (ktr) following a rapid release and restretch is determined by the maximal rate of cross-bridge cycling. During submaximal Ca2+ activations, however, ktr regulation varies with thin filament dynamics. Thus, decreasing the rate of Ca2+ dissociation from TnC produces a higher ktr value at a given tension level (P), especially in the [Ca2+] range that yields less than 50% of maximal tension (Po). In this study, native rabbit TnC was replaced with chicken recombinant TnC, either wild-type (rTnC) or mutant (NHdel), with decreased Ca2+ affinity and an increased Ca2+ dissociation rate (koff). Despite marked differences in Ca2+ sensitivity (>0.5 DeltapCa50), fibers reconstituted with either of the recombinant proteins exhibited similar ktr versus tension profiles, with ktr low (1-2 s-1) and constant up to approximately 50% Po, then rising sharply to a maximum (16 +/- 0.8 s-1) in fully activated fibers. This behavior is predicted by a four-state model based on coupling between cross-bridge cycling and thin filament regulation, where Ca2+ directly affects only individual thin filament regulatory units. These data and model simulations confirm that the range of ktr values obtained with varying Ca2+ can be regulated by a rate-limiting thin filament process.
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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.