ArticleThe Journal of physiology2002
Troponin I phosphorylation enhances crossbridge kinetics during beta-adrenergic stimulation in rat cardiac tissue.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Research into the physiology of myosins - a personal odyssey.European journal of translational myology · 2025Article
- Differential changes in cyclic adenosine 3'-5' monophosphate (cAMP) effectors and major CaJournal of cellular and molecular medicine · 2023Article
- Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling.Scientific reports · 2016Article
- Cardiac troponin structure-function and the influence of hypertrophic cardiomyopathy associated mutations on modulation of contractility.Archives of biochemistry and biophysics · 2016Review
- Insights into length-dependent regulation of cardiac cross-bridge cycling kinetics in human myocardium.Archives of biochemistry and biophysics · 2016Article
- X-ray diffraction analysis of the effects of myosin regulatory light chain phosphorylation and butanedione monoxime on skinned skeletal muscle fibers.American journal of physiology. Cell physiology · 2016Article
- Alterations in Multi-Scale Cardiac Architecture in Association With Phosphorylation of Myosin Binding Protein-C.Journal of the American Heart Association · 2016Article
- CaMKII-dependent myofilament Ca2+ desensitization contributes to the frequency-dependent acceleration of relaxation.Cell calcium · 2015Article
- Tri-modal regulation of cardiac muscle relaxation; intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.Biophysical reviews · 2014Article
- Impact of site-specific phosphorylation of protein kinase A sites Ser23 and Ser24 of cardiac troponin I in human cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2013Article
- Cardiac myosin isoforms exhibit differential rates of MgADP release and MgATP binding detected by myocardial viscoelasticity.Journal of molecular and cellular cardiology · 2013Article
- Alanine or aspartic acid substitutions at serine23/24 of cardiac troponin I decrease thin filament activation, with no effect on crossbridge detachment kinetics.Archives of biochemistry and biophysics · 2012Article
- Magnitude of length-dependent changes in contractile properties varies with titin isoform in rat ventricles.American journal of physiology. Heart and circulatory physiology · 2012Article
- Protein kinase A changes calcium sensitivity but not crossbridge kinetics in human cardiac myofibrils.American journal of physiology. Heart and circulatory physiology · 2011Article
- Protein kinase A-induced myofilament desensitization to Ca(2+) as a result of phosphorylation of cardiac myosin-binding protein C.The Journal of general physiology · 2010Article
- Expression of masticatory-specific isoforms of myosin heavy-chain, myosin-binding protein-C and tropomyosin in muscle fibers and satellite cell cultures of cat masticatory muscle.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010Article
- Protein kinase A-dependent modulation of Ca2+ sensitivity in cardiac and fast skeletal muscles after reconstitution with cardiac troponin.The Journal of general physiology · 2009Article
- Role of the acidic N' region of cardiac troponin I in regulating myocardial function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008Article
- Acceleration of stretch activation in murine myocardium due to phosphorylation of myosin regulatory light chain.The Journal of general physiology · 2006Article
- Phosphorylation of titin modulates passive stiffness of cardiac muscle in a titin isoform-dependent manner.The Journal of general physiology · 2005Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inotropic agents that increase the intracellular levels of cAMP have been shown to increase crossbridge turnover kinetics in intact rat ventricular muscle, as measured by the parameter f(min) (the frequency at which dynamic stiffness is minimum). These agents are also known to increase the level of phosphorylation of two candidate myofibrillar proteins: myosin binding protein C (MyBPC) and Troponin I (TnI), but have no effect on myosin light chain 2 phosphorylation (MyLC2). The aim of this study was to investigate whether the phosphorylation of TnI and/or MyBPC was responsible for the increase in crossbridge cycling kinetics (as captured by f(min)) seen with the elevation of cAMP within cardiac tissue. Using barium-activated intact rat papillary muscle, we investigated the actions of isobutylmethylxanthine (IBMX), an inhibitor of cAMP-dependent phosphatase, which simulates the action of beta-adrenergic agents, and the chemical phosphatase 2,3-butanedione monoxime (BDM), which has been shown to dephosphorylate a number of contractile proteins. The presence of 0.6 mM IBMX approximately doubled the f(min) value of intact rat papillary muscle. This action was unaffected by the addition of BDM. In the presence of IBMX and BDM, the level of phosphorylation of MyBPC was unchanged, that of MyLC2 was reduced to 60 % of control, yet that of TnI was markedly increased (to 30 % above control levels). We conclude that TnI phosphorylation, mediated by cAMP-dependent protein kinase A, is the molecular basis for the enhanced crossbridge cycling seen during beta-adrenergic stimulation of the heart.
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