ReviewPflugers Archiv : European journal of physiology2014
Post-translational control of cardiac hemodynamics through myosin binding protein C.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- LncRNA Foxo6os as a Novel " Scaffold" Mediates MYBPC3 in Combating Pathological Cardiac Hypertrophy and Heart Failure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Myosin binding protein-C modulates loaded sarcomere shortening in rodent permeabilized cardiac myocytes.The Journal of general physiology · 2025Article
- Post-translational modifications of vertebrate striated muscle myosin heavy chains.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Article
- Negative inotropic mechanisms of β-cardiotoxin in cardiomyocytes by depression of myofilament ATPase activity without activation of the classical β-adrenergic pathway.Scientific reports · 2021Article
- Molecular Genetic Basis of Hypertrophic Cardiomyopathy.Circulation research · 2021Article
- A feline orthologue of the human MYH7 c.5647G>A (p.(Glu1883Lys)) variant causes hypertrophic cardiomyopathy in a Domestic Shorthair cat.European journal of human genetics : EJHG · 2019Article
- Cardiac myosin-binding protein C is a novel marker of myocardial injury and fibrosis in aortic stenosis.Heart (British Cardiac Society) · 2018Article
- Structure before function: myosin binding protein-C slow is a structural protein with regulatory properties.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Peroxisome proliferator-activated receptor-α expression induces alterations in cardiac myofilaments in a pressure-overload model of hypertrophy.American journal of physiology. Heart and circulatory physiology · 2017Article
- Role of myosin light chain phosphatase in cardiac physiology and pathophysiology.Journal of molecular and cellular cardiology · 2016Review
- Phosphorylation of cardiac myosin binding protein-C regulates heart contraction and dilatation in vivo during β-adrenergic receptor activation.The Journal of physiology · 2016Article
- Myosin light chain phosphorylation enhances contraction of heart muscle via structural changes in both thick and thin filaments.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- MYBPC1, an Emerging Myopathic Gene: What We Know and What We Need to Learn.Frontiers in physiology · 2016Review
- Review
- Convergent evolution of marine mammals is associated with distinct substitutions in common genes.Scientific reports · 2015Article
- Orientation of myosin binding protein C in the cardiac muscle sarcomere determined by domain-specific immuno-EM.Journal of molecular biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac myosin binding protein C (cMyBP-C) is an integral sarcomeric protein that associates with the thick, thin, and titin filament systems in the contractile apparatus. Three different isoforms of MyBP-C exist in mammalian muscle: slow skeletal (MyBPC1), fast skeletal (MyBP-C2, with several variants), and cardiac (cMyBP-C). Genetic screening studies show that mutations in MYBPC3 occur frequently and are responsible for as many as 30-35 % of identified cases of familial hypertrophic cardiomyopathy. The function of cMyBP-C is stringently regulated by its post-translational modification. In particular, the addition of phosphate groups occurs with high frequency on certain serine residues that are located in the cardiac-specific regulatory M domain. Phosphorylation of this domain has been extensively studied in vitro and in vivo. Phosphorylation of the M domain can regulate the manner in which actin and myosin interact, affecting the cross bridge cycle and ultimately, cardiac hemodynamics.
Indexed as
Identifiers
What OpenQuestion holds
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.