ReviewPflugers Archiv : European journal of physiology2014
Cardiac myosin binding protein-C as a central target of cardiac sarcomere signaling: a special mini review series.
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 26 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
26 citing papers in PubMed, 42 citations in OpenAlex.
- MMP-9 Gene Ablation Preserves Ejection Fraction During "Single-Hit" Model of HFrEF.Biochemical genetics · 2026Article
- LncRNA Foxo6os as a Novel " Scaffold" Mediates MYBPC3 in Combating Pathological Cardiac Hypertrophy and Heart Failure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Influence of Soluble Guanylate Cyclase on Cardiac, Vascular, and Renal Structure and Function: A Physiopathological Insight.International journal of molecular sciences · 2025Review
- Bringing into focus the central domains C3-C6 of myosin binding protein C.Frontiers in physiology · 2024Review
- Mitochondrial and Proteasome Dysfunction Occurs in the Hearts of Mice Treated with Triazine Herbicide Prometryn.International journal of molecular sciences · 2023Article
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- Protein haploinsufficiency drivers identify MYBPC3 variants that cause hypertrophic cardiomyopathy.The Journal of biological chemistry · 2021Article
- Genetic, clinical, molecular, and pathogenic aspects of the South Asian-specific polymorphic MYBPC3Biophysical reviews · 2020Review
- Sarcomeric Gene Variants and Their Role with Left Ventricular Dysfunction in Background of Coronary Artery Disease.Biomolecules · 2020Review
- Bayesian inference of protein conformational ensembles from limited structural data.PLoS computational biology · 2018Article
- Interaction between cardiac myosin-binding protein C and formin Fhod3.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- My Life, My Heart, and My(osin) Binding Protein-C.Circulation research · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Skeletal myosin binding protein-C isoforms regulate thin filament activity in a CaScientific reports · 2018Article
- Titin stiffness modifies the force-generating region of muscle sarcomeres.Scientific reports · 2016Article
- The development and application of a high-sensitivity immunoassay for cardiac myosin-binding protein C.Translational research : the journal of laboratory and clinical medicine · 2016Article
- Phosphorylation and calcium antagonistically tune myosin-binding protein C's structure and function.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Titin strain contributes to the Frank-Starling law of the heart by structural rearrangements of both thin- and thick-filament proteins.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The cMyBP-C HCM variant L348P enhances thin filament activation through an increased shift in tropomyosin position.Journal of molecular and cellular cardiology · 2016Article
- Should we treat heart failure with phosphatase inhibitors? Better to start at the end.Journal of molecular and cellular cardiology · 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 a cardiac-specific thick filament assembly, accessory, and regulatory protein. Physiologically, it is a key regulator of cardiac contractility. With more than 200 mutations in the cMyBP-C gene directly linked to the development of cardiomyopathy and heart failure, cMyBP-C clearly plays a critical role in heart function. At baseline, cMyBP-C is highly phosphorylated, a condition required for normal cardiac function. However, the level of cMyBP-C phosphorylation is significantly decreased during heart failure, indicating that the level of cMyBP-C phosphorylation is directly linked to signaling and cardiac function. Early studies indicated that cMyBP-C interacts with myosin and titin, whereas studies now show that it also interacts with thin filament proteins. However, the exact role(s) of cMyBP-C in the heart remain(s) to be elucidated. As such, we invited experts in the field of cardiac muscle to identify and address key issues related to cMyBP-C by contributing a mini review on such topics as structure, function, regulation, cardiomyopathy, proteolysis, and gene therapy. Starting from this issue, Pflügers Archiv European Journal of Physiology will publish two invited mini review articles each month to discuss the most recent advances in the study of cMyBP-C.
Indexed as
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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.