ReviewJournal of muscle research and cell motility2012
Cardiac myosin binding protein C phosphorylation in cardiac disease.
Review in Journal of muscle research and cell motility, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 56 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
- cMyBP-C in hypertrophic cardiomyopathy: gene therapy and small-molecule innovations.Frontiers in cardiovascular medicine · 2025Review
- Roles of cMyBP-C phosphorylation on cardiac contractile dysfunction inJournal of molecular and cellular cardiology plus · 2024Article
- The Relationship between Changes inJournal of cardiovascular development and disease · 2023Review
- Distinct Mechanisms for Increased Cardiac Contraction Through Selective Alteration of Either Myosin or Troponin Activity.JACC. Basic to translational science · 2022Article
- Article
- Inhibiting cardiac myeloperoxidase alleviates the relaxation defect in hypertrophic cardiomyocytes.Cardiovascular research · 2022Article
- Hypertrophic cardiomyopathy: Mutations to mechanisms to therapies.Frontiers in physiology · 2022Review
- Functional and Molecular Characterisation of Heart Failure Progression in Mice and the Role of Myosin Regulatory Light Chains in the Recovery of Cardiac Muscle Function.International journal of molecular sciences · 2021Article
- Assessment of the Contribution of a Thermodynamic and Mechanical Destabilization of Myosin-Binding Protein C Domain C2 to the Pathomechanism of Hypertrophic Cardiomyopathy-Causing Double MutationInternational journal of molecular sciences · 2021Article
- Mechanisms of Systolic Cardiac Dysfunction in PP2A, PP5 and PP2AxPP5 Double Transgenic Mice.International journal of molecular sciences · 2021Article
- The Interplay between S-Glutathionylation and Phosphorylation of Cardiac Troponin I and Myosin Binding Protein C in End-Stage Human Failing Hearts.Antioxidants (Basel, Switzerland) · 2021Article
- Regulation of Cardiac PKA Signaling by cAMP and Oxidants.Antioxidants (Basel, Switzerland) · 2021Review
- Receptor-independent modulation of cAMP-dependent protein kinase and protein phosphatase signaling in cardiac myocytes by oxidizing agents.The Journal of biological chemistry · 2020Article
- A Novel "Cut and Paste" Method for In Situ Replacement of cMyBP-C Reveals a New Role for cMyBP-C in the Regulation of Contractile Oscillations.Circulation research · 2020Article
- Serine/Threonine Phosphatases in Atrial Fibrillation.Journal of molecular and cellular cardiology · 2017Review
- Roles and regulation of protein phosphatase 2A (PP2A) in the heart.Journal of molecular and cellular cardiology · 2016Review
- Deletion of Pr130 Interrupts Cardiac Development in Zebrafish.International journal of molecular sciences · 2016Article
- S-glutathiolation impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perturbations in sarcomeric function may in part underlie systolic and diastolic dysfunction of the failing heart. Sarcomeric dysfunction has been ascribed to changes in phosphorylation status of sarcomeric proteins caused by an altered balance between intracellular kinases and phosphatases during the development of cardiac disease. In the present review we discuss changes in phosphorylation of the thick filament protein myosin binding protein C (cMyBP-C) reported in failing myocardium, with emphasis on phosphorylation changes observed in familial hypertrophic cardiomyopathy caused by mutations in MYBPC3. Moreover, we will discuss assays which allow to distinguish between functional consequences of mutant sarcomeric proteins and (mal)adaptive changes in sarcomeric protein phosphorylation.
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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.