ArticleBiophysical journal2012
The C-terminus of troponin T is essential for maintaining the inactive state of regulated actin.
Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
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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
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- Hypertrophic Cardiomyopathy Mutations of Troponin Reveal Details of Striated Muscle Regulation.Frontiers in physiology · 2022Pooled it
- Meta-analysis of cardiomyopathy-associated variants in troponin genes identifies loci and intragenic hot spots that are associated with worse clinical outcomes.Journal of molecular and cellular cardiology · 2020Pooled it
- Resolving the structure and dynamics of the disordered C terminus of human cardiac troponin T and effects of cardiomyopathic mutations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The highly conserved C-terminal end segment of troponin T binds tropomyosin and actin to function in modulating contractile kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Glutamate 139 of tropomyosin is critical for cardiac thin filament blocked-state stabilization.Journal of molecular and cellular cardiology · 2024Article
- Negative Charges Introduced Near the IT Helix of Cardiac Troponin T Stabilize the Active State of Actin Filaments.Biochemistry · 2023Article
- 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
- Low expression of the K280NJournal of molecular and cellular cardiology plus · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Significance of Cardiac Troponins as an Identification Tool in COVID-19 Patients Using Biosensors: An Update.Frontiers in molecular biosciences · 2022Review
- 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
- Ovine congenital progressive muscular dystrophy (OCPMD) is a model of TNNT1 congenital myopathy.Acta neuropathologica communications · 2020Article
- Troponin structure and function: a view of recent progress.Journal of muscle research and cell motility · 2020Review
- The intrinsically disordered C terminus of troponin T binds to troponin C to modulate myocardial force generation.The Journal of biological chemistry · 2019Article
- Basic residues within the cardiac troponin T C terminus are required for full inhibition of muscle contraction and limit activation by calcium.The Journal of biological chemistry · 2019Article
- Stepwise C-Terminal Truncation of Cardiac Troponin T Alters Function at Low and Saturating CaBiophysical journal · 2018Article
- Multiple Species Comparison of Cardiac Troponin T and Dystrophin: Unravelling the DNA behind Dilated Cardiomyopathy.Journal of cardiovascular development and disease · 2017Review
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Troponin C Mutations Partially Stabilize the Active State of Regulated Actin and Fully Stabilize the Active State When Paired with Δ14 TnT.Biochemistry · 2017Article
- Commentary: Effect of Skeletal Muscle Native Tropomyosin on the Interaction of Amoeba Actin with Heavy Meromyosin.Frontiers in physiology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Striated muscle contraction is regulated by the actin binding proteins tropomyosin and troponin. Defects in these proteins lead to myopathies and cardiomyopathies. Deletion of the 14 C-terminal residues of cardiac troponin T leads to hypertrophic cardiomyopathy. We showed earlier that regulated actin containing Δ14 TnT was more readily activated than wild-type regulated actin. We suggested that the equilibria among the inactive (blocked), intermediate (closed or calcium), and active (open or myosin) states was shifted to the active state. We now show that, in addition, such regulated actin filaments cannot enter the inactive or blocked state. Regulated actin containing Δ14 TnT had ATPase activities in the absence of Ca2+ that were higher than wild-type filaments but far below the fully active rate. The rapid dissociation of S1-ATP from regulated actin filaments containing Δ14 TnT and acrylodan-labeled tropomyosin did not show the fluorescence increase characteristic of moving to the inactive state. Replacing wild-type TnI with S45E TnI, that favors the inactive state, did not restore the fluorescence change. We conclude that TnT has a previously unrecognized role in forming the inactive state of regulated actin.
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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.