ArticleBiophysical journal2012
The N-terminal extension of cardiac troponin T stabilizes the blocked state of cardiac thin filament.
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 31 papers.
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Who cites it
31 citing papers in PubMed, 39 citations in OpenAlex.
- Significance of Cardiac Troponins as an Identification Tool in COVID-19 Patients Using Biosensors: An Update.Frontiers in molecular biosciences · 2022Review
- The actin 'A-triad's' role in contractile regulation in health and disease.The Journal of physiology · 2020Review
- Deletion of Enigma Homologue from the Z-disc slows tension development kinetics in mouse myocardium.The Journal of general physiology · 2019Article
- Cardiomyopathy mutation (F88L) in troponin T abolishes length dependency of myofilament CaThe Journal of general physiology · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Omecamtiv Mecarbil Abolishes Length-Mediated Increase in Guinea Pig Cardiac Myofiber CaBiophysical journal · 2017Article
- Cardiac myosin binding protein-C SerScience advances · 2017Article
- Hypertrophic Cardiomyopathy Cardiac Troponin C Mutations Differentially Affect Slow Skeletal and Cardiac Muscle Regulation.Frontiers in physiology · 2017Article
- L71F mutation in rat cardiac troponin T augments crossbridge recruitment and detachment dynamics against α-myosin heavy chain, but not against β-myosin heavy chain.Journal of muscle research and cell motility · 2016Article
- The effect of cardiomyopathy mutation (R97L) in mouse cardiac troponin T on the muscle length-mediated recruitment of crossbridges is modified divergently by α- and β-myosin heavy chain.Archives of biochemistry and biophysics · 2016Article
- Interplay between the effects of a Protein Kinase C phosphomimic (T204E) and a dilated cardiomyopathy mutation (K211Δ or R206W) in rat cardiac troponin T blunts the magnitude of muscle length-mediated crossbridge recruitment against the β-myosin heavy chain background.Journal of muscle research and cell motility · 2016Article
- Interplay Between the Effects of Dilated Cardiomyopathy Mutation (R206L) and the Protein Kinase C Phosphomimic (T204E) of Rat Cardiac Troponin T Are Differently Modulated by α- and β-Myosin Heavy Chain Isoforms.Journal of the American Heart Association · 2016Article
- Dilated Cardiomyopathy Mutation (R134W) in Mouse Cardiac Troponin T Induces Greater Contractile Deficits against α-Myosin Heavy Chain than against β-Myosin Heavy Chain.Frontiers in physiology · 2016Article
- Cardiac Myosin Binding Protein-C Phosphorylation Modulates Myofilament Length-Dependent Activation.Frontiers in physiology · 2016Article
- ADP-stimulated contraction: A predictor of thin-filament activation in cardiac disease.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Historical perspective on heart function: the Frank-Starling Law.Biophysical reviews · 2015Review
- Rat cardiac troponin T mutation (F72L)-mediated impact on thin filament cooperativity is divergently modulated by α- and β-myosin heavy chain isoforms.American journal of physiology. Heart and circulatory physiology · 2015Article
- The functional effect of dilated cardiomyopathy mutation (R144W) in mouse cardiac troponin T is differently affected by α- and β-myosin heavy chain isoforms.American journal of physiology. Heart and circulatory physiology · 2015Article
- In situ time-resolved FRET reveals effects of sarcomere length on cardiac thin-filament activation.Biophysical journal · 2014Article
- Length-dependent changes in contractile dynamics are blunted due to cardiac myosin binding protein-C ablation.Frontiers in physiology · 2014Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac troponin T (cTnT) is a key component of contractile regulatory proteins. cTnT is characterized by a ∼32 amino acid N-terminal extension (NTE), the function of which remains unknown. To understand its function, we generated a transgenic (TG) mouse line that expressed a recombinant chimeric cTnT in which the NTE of mouse cTnT was removed by replacing its 1-73 residues with the corresponding 1-41 residues of mouse fast skeletal TnT. Detergent-skinned papillary muscle fibers from non-TG (NTG) and TG mouse hearts were used to measure tension, ATPase activity, Ca(2+) sensitivity (pCa(50)) of tension, rate of tension redevelopment, dynamic muscle fiber stiffness, and maximal fiber shortening velocity at sarcomere lengths (SLs) of 1.9 and 2.3 μm. Ca(2+) sensitivity increased significantly in TG fibers at both short SL (pCa(50) of 5.96 vs. 5.62 in NTG fibers) and long SL (pCa(50) of 6.10 vs. 5.76 in NTG fibers). Maximal cross-bridge turnover and detachment kinetics were unaltered in TG fibers. Our data suggest that the NTE constrains cardiac thin filament activation such that the transition of the thin filament from the blocked to the closed state becomes less responsive to Ca(2+). Our finding has implications regarding the effect of tissue- and disease-related changes in cTnT isoforms on cardiac muscle function.
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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.