ArticleArchives of biochemistry and biophysics2012
Alanine or aspartic acid substitutions at serine23/24 of cardiac troponin I decrease thin filament activation, with no effect on crossbridge detachment kinetics.
Article in Archives of biochemistry and biophysics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- The Importance of Intrinsically Disordered Segments of Cardiac Troponin in Modulating Function by Phosphorylation and Disease-Causing Mutations.Frontiers in physiology · 2016Review
- Molecular effects of the myosin activator omecamtiv mecarbil on contractile properties of skinned myocardium lacking cardiac myosin binding protein-C.Journal of molecular and cellular cardiology · 2015Article
- β-adrenergic effects on cardiac myofilaments and contraction in an integrated rabbit ventricular myocyte model.Journal of molecular and cellular cardiology · 2015Article
- Investigating the role of uncoupling of troponin I phosphorylation from changes in myofibrillar Ca(2+)-sensitivity in the pathogenesis of cardiomyopathy.Frontiers in physiology · 2014Review
- Instability in the central region of tropomyosin modulates the function of its overlapping ends.Biophysical journal · 2013Article
- Divergent effects of α- and β-myosin heavy chain isoforms on the N terminus of rat cardiac troponin T.The Journal of general physiology · 2013Article
- Interplay between the overlapping ends of tropomyosin and the N terminus of cardiac troponin T affects tropomyosin states on actin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- New insights into the functional significance of the acidic region of the unique N-terminal extension of cardiac troponin I.Biochimica et biophysica acta · 2013Article
- Identification of two new regions in the N-terminus of cardiac troponin T that have divergent effects on cardiac contractile function.The Journal of physiology · 2013Article
- Integration of troponin I phosphorylation with cardiac regulatory networks.Circulation research · 2013Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Ala/Asp substitutions at Ser23/24 have been employed to investigate the functional impact of cardiac troponin I (cTnI) phosphorylation by protein kinase A (PKA). Some limitations of previous studies include the use of heterologous proteins and confounding effects arising from phosphorylation of cardiac myosin binding protein-C. Our goal was to probe the effects of cTnI phosphorylation using a homologous assay, so that altered function could be solely attributed to changes in cTnI. We reconstituted detergent-skinned rat cardiac papillary fibers with homologous rat cardiac troponin subunits to study the impact of Ala and Asp substitutions at Ser23/24 of rat cTnI (RcTnI S23A/24A and RcTnI S23D/24D). Both RcTnI S23A/24A and RcTnI S23D/24D showed a ~36% decrease in Ca(2+)-activated maximal tension. Both RcTnI S23A/24A and RcTnI S23D/24D showed a ~18% decrease in ATPase activity. Muscle fiber stiffness measurements suggested that the decrease in thin filament activation observed in RcTnI S23A/24A and RcTnI S23D/24D was due to a decrease in the number of strongly-bound crossbridges. Another major finding was that Ala and Asp substitutions in cTnI did not affect crossbridge detachment kinetics.
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