ArticleThe Journal of clinical investigation1996
Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 203 citations in OpenAlex.
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- Effects of Di(2-ethylhexyl) phthalate (DEHP) and hyperoxia on cardiovascular development in newborn rats.Pediatric research · 2026Article
- The Role of MYH6 Variants in atrial cardiomyopathy: insights from clinical observations and zebrafish models.NPJ genomic medicine · 2026Article
- Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.JACC. Basic to translational science · 2025Review
- Slow myosin heavy chain 1 is required for slow myofibril and muscle fibre growth but not for myofibril initiation.Developmental biology · 2023Article
- Sin3a Associated Protein 130kDa, sap130, plays an evolutionary conserved role in zebrafish heart development.bioRxiv : the preprint server for biology · 2023Article
- Sinus node dysfunction: current understanding and future directions.American journal of physiology. Heart and circulatory physiology · 2023Review
- Efficient in vivo genome editing prevents hypertrophic cardiomyopathy in mice.Nature medicine · 2023Article
- Exploring the complex spectrum of dominance and recessiveness in genetic cardiomyopathies.Nature cardiovascular research · 2023Article
- Sin3a associated protein 130 kDa, sap130, plays an evolutionary conserved role in zebrafish heart development.Frontiers in cell and developmental biology · 2023Article
- Visualizing Subcellular Localization of a Protein in the Heart using Quantum Dots-Mediated Immuno-Labeling followed by Transmission Electron Microscopy.Journal of visualized experiments : JoVE · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Adipose Lipolysis Regulates Cardiac Glucose Uptake and Function in Mice under Cold Stress.International journal of molecular sciences · 2021Article
- Biologically Derived, Three-Dimensional, Embryonic Scaffolds for Long-Term Cardiomyocyte Culture.Stem cells and development · 2021Article
- Contraction-relaxation coupling is unaltered by exercise training and infarction in isolated canine myocardium.The Journal of general physiology · 2021Article
- Genetics of Transposition of Great Arteries: Between Laterality Abnormality and Outflow Tract Defect.Journal of cardiovascular translational research · 2021Review
- Genetic Etiology of Left-Sided Obstructive Heart Lesions: A Story in Development.Journal of the American Heart Association · 2021Review
- A Multi-Omics Approach Using a Mouse Model of Cardiac Malformations for Prioritization of Human Congenital Heart Disease Contributing Genes.Frontiers in cardiovascular medicine · 2021Article
- Gene therapy for inherited arrhythmias.Cardiovascular research · 2020Review
- Allele-Selective Knockdown of MYH7 Using Antisense Oligonucleotides.Molecular therapy. Nucleic acids · 2020Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The alpha-myosin heavy chain (alpha-MyHC) is the major contractile protein expressed in the myocardium of adult mice. We have produced mice carrying a null mutation of alpha-MyHC by homologous recombination in murine ES cells. Homozygous null animals die between 11 and 12 d in utero of gross heart defects, while alpha-MyHC+/- heterozygotes survive and appear externally normal. The presence of a single functional alpha-MyHC+ allele in heterozygous animals results in reduced levels of the transcript and protein as well as fibrosis and alterations in sarcomeric structure. Examination of heart function using a working heart preparation revealed severe impairment of both contractility and relaxation in a subset of the alpha-MyHC+/- animals. Thus, two alpha-MyHC+ alleles are necessary for normal cardiac development, and hemizygosity for the normal allele can result in altered cardiac function.
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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.