ReviewJournal of cardiovascular translational research2009
Insights into human beta-cardiac myosin function from single molecule and single cell studies.
Review in Journal of cardiovascular translational research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 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
20 citing papers in PubMed, 30 citations in OpenAlex.
- Understanding hypertrophic cardiomyopathy and its regulation by myosin drugs.Protein science : a publication of the Protein Society · 2025Article
- Reassessing the unifying hypothesis for hypercontractility caused by myosin mutations in hypertrophic cardiomyopathy.The EMBO journal · 2024Review
- Myosin-Catalyzed ATP Hydrolysis in the Presence of Disease-Causing Mutations: Mavacamten as a Way to Repair Mechanism.The journal of physical chemistry. B · 2024Article
- Regional Variation in Cardiovascular Genes Enables a Tractable Genome Editing Strategy.Circulation. Genomic and precision medicine · 2024Article
- Hypertrophic cardiomyopathy: Mutations to mechanisms to therapies.Frontiers in physiology · 2022Review
- Myocardial Contractility: Historical and Contemporary Considerations.Frontiers in physiology · 2020Article
- The Molecular Mechanisms of Mutations in Actin and Myosin that Cause Inherited Myopathy.International journal of molecular sciences · 2018Review
- Adaptation and validation of the ACMG/AMP variant classification framework for MYH7-associated inherited cardiomyopathies: recommendations by ClinGen's Inherited Cardiomyopathy Expert Panel.Genetics in medicine : official journal of the American College of Medical Genetics · 2018Article
- Hypertrophic cardiomyopathy and the myosin mesa: viewing an old disease in a new light.Biophysical reviews · 2018Review
- Insights from molecular dynamics simulations for computational protein design.Molecular systems design & engineering · 2017Article
- Modulating Beta-Cardiac Myosin Function at the Molecular and Tissue Levels.Frontiers in physiology · 2016Article
- Effects of hypertrophic and dilated cardiomyopathy mutations on power output by human β-cardiac myosin.The Journal of experimental biology · 2016Review
- Ensemble force changes that result from human cardiac myosin mutations and a small-molecule effector.Cell reports · 2015Article
- Electrical and Mechanical Strategies to Enable Cardiac Repair and Regeneration.IEEE reviews in biomedical engineering · 2015Review
- Sacrificial layer technique for axial force post assay of immature cardiomyocytes.Biomedical microdevices · 2013Article
- Article
- Subtle abnormalities in contractile function are an early manifestation of sarcomere mutations in dilated cardiomyopathy.Circulation. Cardiovascular genetics · 2012Article
- Cell-intrinsic functional effects of the α-cardiac myosin Arg-403-Gln mutation in familial hypertrophic cardiomyopathy.Biophysical journal · 2012Article
- How do mutations in contractile proteins cause the primary familial cardiomyopathies?Journal of cardiovascular translational research · 2011Review
- Identifying sarcomere gene mutations in hypertrophic cardiomyopathy: a personal history.Circulation research · 2011Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
beta-Cardiac myosin is a mechanoenzyme that converts the energy from ATP hydrolysis into a mechanical force that drives contractility in muscle. Thirty percent of the point mutations that result in hypertrophic cardiomyopathy are localized to MYH7, the gene encoding human beta-cardiac myosin heavy chain (beta-MyHC). Force generation by myosins requires a tight and highly conserved allosteric coupling between its different protein domains. Hence, the effects of single point mutations on the force generation and kinetics of beta-cardiac myosin molecules cannot be predicted directly from their location within the protein structure. Great insight would be gained from understanding the link between the functional defect in the myosin protein and the clinical phenotypes of patients expressing them. Over the last decade, several single molecule techniques have been developed to understand in detail the chemomechanical cycle of different myosins. In this review, we highlight the single molecule techniques that can be used to assess the effect of point mutations on beta-cardiac myosin function. Recent bioengineering advances have enabled the micromanipulation of single cardiomyocyte cells to characterize their force-length dynamics. Here, we briefly review single cell micromanipulation as an approach to determine the effect of beta-MyHC mutations on cardiomyocyte function. Finally, we examine the technical challenges specific to studying beta-cardiac myosin function both using single molecule and single cell approaches.
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.