ArticleThe Journal of physiology2007
Thin-filament regulation of force redevelopment kinetics in rabbit skeletal muscle fibres.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Fluorescent Protein-Based Ca2+ Sensor Reveals Global, Divalent Cation-Dependent Conformational Changes in Cardiac Troponin C.PloS one · 2016Article
- Cell-based delivery of dATP via gap junctions enhances cardiac contractility.Journal of molecular and cellular cardiology · 2014Article
- Diaphragm and ventilatory dysfunction during cancer cachexia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Slowed Dynamics of Thin Filament Regulatory Units Reduces CaCellular and molecular bioengineering · 2013Article
- Article
- Significance of troponin dynamics for Ca2+-mediated regulation of contraction and inherited cardiomyopathy.The Journal of biological chemistry · 2012Article
- 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
- Filament compliance influences cooperative activation of thin filaments and the dynamics of force production in skeletal muscle.PLoS computational biology · 2012Article
- Calcium binding kinetics of troponin C strongly modulate cooperative activation and tension kinetics in cardiac muscle.Journal of molecular and cellular cardiology · 2011Article
- Effect of Ca2+ binding properties of troponin C on rate of skeletal muscle force redevelopment.American journal of physiology. Cell physiology · 2010Article
- Prolonged space flight-induced alterations in the structure and function of human skeletal muscle fibres.The Journal of physiology · 2010Article
- Myofilament length dependent activation.Journal of molecular and cellular cardiology · 2010Review
- 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
- Tropomyosin in the groove? Molecular insights into an inherited myopathy.The Journal of physiology · 2007Article
- The effects of force inhibition by sodium vanadate on cross-bridge binding, force redevelopment, and Ca2+ activation in cardiac muscle.Biophysical journal · 2007Article
- Investigation of thin filament near-neighbour regulatory unit interactions during force development in skinned cardiac and skeletal muscle.The Journal of physiology · 2007Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Thin-filament regulation of isometric force redevelopment (k(tr)) was examined in rabbit psoas fibres by substituting native TnC with either cardiac TnC (cTnC), a site I-inactive skeletal TnC mutant (xsTnC), or mixtures of native purified skeletal TnC (sTnC) and a site I- and II-inactive skeletal TnC mutant (xxsTnC). Reconstituted maximal Ca(2+)-activated force (rF(max)) decreased as the fraction of sTnC in sTnC: xxsTnC mixtures was reduced, but maximal k(tr) was unaffected until rF(max) was <0.2 of pre-extracted F(max). In contrast, reconstitution with cTnC or xsTnC reduced maximal k(tr) to 0.48 and 0.44 of control (P < 0.01), respectively, with corresponding rF(max) of 0.68 +/- 0.03 and 0.25 +/- 0.02 F(max). The k(tr)-pCa relation of fibres containing sTnC: xxsTnC mixtures (rF(max) > 0.2 F(max)) was little effected, though k(tr) was slightly elevated at low Ca(2+) activation. The magnitude of the Ca(2+)-dependent increase in k(tr) was greatly reduced following cTnC or xsTnC reconstitution because k(tr) at low levels of Ca(2+) was elevated and maximal k(tr) was reduced. Solution Ca(2+) dissociation rates (k(off)) from whole Tn complexes containing sTnC (26 +/- 0.1 s(-1)), cTnC (38 +/- 0.9 s(-1)) and xsTnC (50 +/- 1.2 s(-1)) correlated with k(tr) at low Ca(2+) levels and were inversely related to rF(max). At low Ca(2+) activation, k(tr) was similarly elevated in cTnC-reconstituted fibres with ATP or when cross-bridge cycling rate was increased with 2-deoxy-ATP. Our results and model simulations indicate little or no requirement for cooperative interactions between thin-filament regulatory units in modulating k(tr) at any [Ca(2+)] and suggest Ca(2+) activation properties of individual troponin complexes may influence the apparent rate constant of cross-bridge detachment.
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