ArticleThe Journal of physiology2006
Ca2+ sensitivity of regulated cardiac thin filament sliding does not depend on myosin isoform.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Actomyosin-Based Nanodevices for Sensing and Actuation: Bridging Biology and Bioengineering.Biosensors · 2025Review
- Post-translational modifications of vertebrate striated muscle myosin heavy chains.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Alpha and beta myosin isoforms and human atrial and ventricular contraction.Cellular and molecular life sciences : CMLS · 2021Review
- Site-specific acetyl-mimetic modification of cardiac troponin I modulates myofilament relaxation and calcium sensitivity.Journal of molecular and cellular cardiology · 2020Article
- Microscopic heat pulses activate cardiac thin filaments.The Journal of general physiology · 2019Article
- Functional significance of HCM mutants of tropomyosin, V95A and D175N, studied withBiophysics and physicobiology · 2019Article
- Article
- Role of cardiac troponin I carboxy terminal mobile domain and linker sequence in regulating cardiac contraction.Archives of biochemistry and biophysics · 2016Article
- The functional significance of the last 5 residues of the C-terminus of cardiac troponin I.Archives of biochemistry and biophysics · 2016Article
- Fluorescent Protein-Based Ca2+ Sensor Reveals Global, Divalent Cation-Dependent Conformational Changes in Cardiac Troponin C.PloS one · 2016Article
- Knock-in mice harboring a Ca(2+) desensitizing mutation in cardiac troponin C develop early onset dilated cardiomyopathy.Frontiers in physiology · 2015Article
- Nuclear tropomyosin and troponin in striated muscle: new roles in a new locale?Journal of muscle research and cell motility · 2013Review
- Slowed Dynamics of Thin Filament Regulatory Units Reduces CaCellular and molecular bioengineering · 2013Article
- Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α-tropomyosin.FEBS letters · 2012Article
- Persistence length of human cardiac α-tropomyosin measured by single molecule direct probe microscopy.PloS one · 2012Article
- Micromechanical thermal assays of Ca2+-regulated thin-filament function and modulation by hypertrophic cardiomyopathy mutants of human cardiac troponin.Journal of biomedicine & biotechnology · 2012Article
- Interaction between troponin and myosin enhances contractile activity of myosin in cardiac muscle.DNA and cell biology · 2011Article
- Several cardiomyopathy causing mutations on tropomyosin either destabilize the active state of actomyosin or alter the binding properties of tropomyosin.Biochemical and biophysical research communications · 2011Article
- Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations.Biophysical journal · 2011Article
- Dynamics of tropomyosin in muscle fibers as monitored by saturation transfer EPR of bi-functional probe.PloS one · 2011Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Myosin heavy chain (MHC) isoforms in vertebrate striated muscles are distinguished functionally by differences in chemomechanical kinetics. These kinetic differences may influence the cross-bridge-dependent co-operativity of thin filament Ca(2+) activation. To determine whether Ca(2+) sensitivity of unloaded thin filament sliding depends upon MHC isoform kinetics, we performed in vitro motility assays with rabbit skeletal heavy meromyosin (rsHMM) or porcine cardiac myosin (pcMyosin). Regulated thin filaments were reconstituted with recombinant human cardiac troponin (rhcTn) and alpha-tropomyosin (rhcTm) expressed in Escherichia coli. All three subunits of rhcTn were coexpressed as a functional complex using a novel construct with a glutathione S-transferase (GST) affinity tag at the N-terminus of human cardiac troponin T (hcTnT) and an intervening tobacco etch virus (TEV) protease site that allows purification of rhcTn without denaturation, and removal of the GST tag without proteolysis of rhcTn subunits. Use of this highly purified rhcTn in our motility studies resulted in a clear definition of the regulated motility profile for both fast and slow MHC isoforms. Maximum sliding speed (pCa 5) of regulated thin filaments was roughly fivefold faster with rsHMM compared with pcMyosin, although speed was increased by 1.6- to 1.9-fold for regulated over unregulated actin with both MHC isoforms. The Ca(2+) sensitivity of regulated thin filament sliding speed was unaffected by MHC isoform. Our motility results suggest that the cellular changes in isoform expression that result in regulation of myosin kinetics can occur independently of changes that influence thin filament Ca(2+) sensitivity.
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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.