ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Protein kinase A changes calcium sensitivity but not crossbridge kinetics in human cardiac myofibrils.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Cardiac Troponin C E135A Variant Impairs Myofilament Response to PKA Phosphorylation and Is Associated With Autosomal Dominant Dilated Cardiomyopathy With Diastolic Dysfunction.Circulation. Genomic and precision medicine · 2025Article
- The relation between sarcomere energetics and the rate of isometric tension relaxation in healthy and diseased cardiac muscle.Journal of muscle research and cell motility · 2021Article
- Article
- Haploinsufficiency of mechanistic target of rapamycin amelioratesDisease models & mechanisms · 2019Article
- The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM.The Journal of general physiology · 2019Article
- A Novel Method of Isolating Myofibrils From Primary Cardiomyocyte Culture Suitable for Myofibril Mechanical Study.Frontiers in cardiovascular medicine · 2019Article
- Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes.Scientific reports · 2017Article
- Transcriptome and Functional Profile of Cardiac Myocytes Is Influenced by Biological Sex.Circulation. Cardiovascular genetics · 2017Article
- Differences in Contractile Function of Myofibrils within Human Embryonic Stem Cell-Derived Cardiomyocytes vs. Adult Ventricular Myofibrils Are Related to Distinct Sarcomeric Protein Isoforms.Frontiers in physiology · 2017Article
- Restrictive Cardiomyopathy Troponin I R145W Mutation Does Not Perturb Myofilament Length-dependent Activation in Human Cardiac Sarcomeres.The Journal of biological chemistry · 2016Article
- Cardiac Myosin Binding Protein-C Phosphorylation Modulates Myofilament Length-Dependent Activation.Frontiers in physiology · 2016Article
- Pacemaker-induced transient asynchrony suppresses heart failure progression.Science translational medicine · 2015Article
- The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I.Biophysical journal · 2014Article
- PKA phosphorylation of cardiac troponin I modulates activation and relaxation kinetics of ventricular myofibrils.Biophysical journal · 2014Article
- The contribution of cardiac myosin binding protein-c Ser282 phosphorylation to the rate of force generation and in vivo cardiac contractility.The Journal of physiology · 2014Article
- Functional dissection of myosin binding protein C phosphorylation.Journal of molecular and cellular cardiology · 2013Article
- Calcium sensitivity and myofilament lattice structure in titin N2B KO mice.Archives of biochemistry and biophysics · 2013Article
- Integration of troponin I phosphorylation with cardiac regulatory networks.Circulation research · 2013Review
- 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 binding protein C and its phosphorylation regulate multiple steps in the cross-bridge cycle of muscle contraction.Biochemistry · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
We investigated the effect of PKA treatment (1 U/ml) on the mechanical properties of isolated human cardiac myofibrils. PKA treatment was associated with significant incorporation of radiolabeled phosphate into several sarcomeric proteins including troponin I and myosin binding protein C and was also associated with a right shift in the tension-pCa relation (ΔpCa(50) = 0.2 ± 0.1). PKA treatment also caused right shifts in the pCa dependence of the rate of tension development, tension redevelopment, and the linear and exponential phases of myofibril relaxation. However, there was no change in the same measures of crossbridge turnover when expressed as a function of tension. We conclude that the changes in crossbridge kinetics as a function of calcium concentration reflect a reduced tension due to a lower calcium sensitivity and that the relationship between crossbridge kinetics and tension was unchanged, indicating no direct effect of PKA treatment on crossbridge cycling.
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Registered trials
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.