ReviewJournal of muscle research and cell motility2012
Myosin binding protein C: implications for signal-transduction.
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 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, 37 citations in OpenAlex.
- Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024Article
- Methods for assessing cardiac myofilament calcium sensitivity.Frontiers in physiology · 2023Review
- Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Why exercise builds muscles: titin mechanosensing controls skeletal muscle growth under load.Biophysical journal · 2021Article
- Shared Molecular Mechanisms of Hypertrophic Cardiomyopathy and Its Clinical Presentations: Automated Molecular Mechanisms Extraction Approach.Life (Basel, Switzerland) · 2021Article
- The updated view on induced pluripotent stem cells for cardiovascular precision medicine.Pflugers Archiv : European journal of physiology · 2021Review
- An interesting Mybpc3 heterozygous mutation associated with bicuspid aortic valve.Translational pediatrics · 2020Article
- Genetic, clinical, molecular, and pathogenic aspects of the South Asian-specific polymorphic MYBPC3Biophysical reviews · 2020Review
- Inguinal Ring RNA Sequencing Reveals Downregulation of Muscular Genes Related to Scrotal Hernia in Pigs.Genes · 2020Article
- Association of Cardiomyopathy With MYBPC3 D389V and MYBPC3Δ25bpIntronic Deletion in South Asian Descendants.JAMA cardiology · 2018Article
- Understanding cardiomyocyte proliferation: an insight into cell cycle activity.Cellular and molecular life sciences : CMLS · 2017Review
- Cardiac myosin binding protein-C as a central target of cardiac sarcomere signaling: a special mini review series.Pflugers Archiv : European journal of physiology · 2014Review
- Gene expression profiles in engineered cardiac tissues respond to mechanical loading and inhibition of tyrosine kinases.Physiological reports · 2013Article
- Force enhancement in lengthening contractions of cat soleus muscle in situ: transient and steady-state aspects.Physiological reports · 2013Article
- Article
- Introducing a series of topical special issues of the Journal of Muscle Research and Cell Motility: MYBPC3 special issue editorial.Journal of muscle research and cell motility · 2012Article
- Structure, interactions and function of the N-terminus of cardiac myosin binding protein C (MyBP-C): who does what, with what, and to whom?Journal of muscle research and cell motility · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
Abstract
Myosin binding protein C (MYBPC) is a crucial component of the sarcomere and an important regulator of muscle function. While mutations in different myosin binding protein C (MYBPC) genes are well known causes of various human diseases, such as hypertrophic (HCM) and dilated (DCM) forms of cardiomyopathy as well as skeletal muscular disorders, the underlying molecular mechanisms remain not well understood. A variety of MYBPC3 (cardiac isoform) mutations have been studied in great detail and several corresponding genetically altered mouse models have been generated. Most MYBPC3 mutations may cause haploinsufficiency and with it they may cause a primary increase in calcium sensitivity which is potentially able to explain major features observed in HCM patients such as the hypercontractile phenotype and the well known secondary effects such as myofibrillar disarray, fibrosis, myocardial hypertrophy and remodelling including arrhythmogenesis. However the presence of poison peptides in some cases cannot be fully excluded and most probably other mechanisms are also at play. Here we shall discuss MYBPC interacting proteins and possible pathways linked to cardiomyopathy and heart failure.
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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.