ArticleTransgenic research1999
Transgenic over-expression of a motor protein at high levels results in severe cardiac pathology.
Article in Transgenic research, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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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.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Long-Term Dystrophin Replacement Therapy in Duchenne Muscular Dystrophy Causes Cardiac Inflammation.JACC. Basic to translational science · 2025Article
- Is developmental plasticity triggered by DNA methylation changes in the invasive cane toad (Ecology and evolution · 2024Article
- Phosphomimetic cardiac myosin-binding protein C partially rescues a cardiomyopathy phenotype in murine engineered heart tissue.Scientific reports · 2019Article
- Homozygous CREM-IbΔC-X Overexpressing Mice Are a Reliable and Effective Disease Model for Atrial Fibrillation.Frontiers in pharmacology · 2018Article
- Healing a Heart Through Genetic Intervention.Circulation research · 2016Article
- 100-fold but not 50-fold dystrophin overexpression aggravates electrocardiographic defects in the mdx model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2016Article
- Characterization of stable fluorescent transgenic marine medaka (Oryzias dancena) lines carrying red fluorescent protein gene driven by myosin light chain 2 promoter.Transgenic research · 2013Article
- Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.Circulation research · 2012Review
- Functional ability of cytoskeletal β-actin regulator to drive constitutive and ubiquitous expression of a fluorescent reporter throughout the life cycle of transgenic marine medaka Oryzias dancena.Transgenic research · 2011Article
- Tissue specific promoters improve specificity of AAV9 mediated transgene expression following intra-vascular gene delivery in neonatal mice.Genetic vaccines and therapy · 2008Article
- Genetic approaches for changing the heart and dissecting complex syndromes.Journal of molecular and cellular cardiology · 2008Review
- Challenges and opportunities in dystrophin-deficient cardiomyopathy gene therapy.Human molecular genetics · 2006Review
- Forced expression of alpha-myosin heavy chain in the rabbit ventricle results in cardioprotection under cardiomyopathic conditions.Circulation · 2005Article
- Functional characterization of the human atrial essential myosin light chain (hALC-1) in a transgenic rat model.Journal of molecular medicine (Berlin, Germany) · 2004Article
- Cardiac expression of Gal4 causes cardiomyopathy in a dose-dependent manner.Journal of muscle research and cell motility · 2003Article
- Meeting Koch's postulates for calcium signaling in cardiac hypertrophy.The Journal of clinical investigation · 2000Review
- Altered focal adhesion regulation correlates with cardiomyopathy in mice expressing constitutively active rac1.The Journal of clinical investigation · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Transgenesis has become a useful tool in effecting a complete or partial remodeling of the cardiac contractile apparatus. Although gene dosage effects were initially a concern, recent data showed that the heart is able to accommodate varying levels of transgenic over-expression without detectable ill effects. The present study was designed to test the limits of the transgenic paradigm in terms of the production of a cardiac phenotype due simply to the over-expression of a contractile protein. To this end, eight lines of mice which express an isoform of the essential myosin light chain 1 that is normally found in the adult ventricle (ELC1v) were generated. Overt phenotype was correlated both with the level of expression/protein replacement and copy number of the transgene. Two of the lines showed essentially complete replacement of the atrial isoform (ELC1a) with ELC1v. However, the phenotypes of the two lines differed dramatically. The line with the lower copy number (37 copies), and moderate over-expression (16 fold) showed no overt pathology while a line with very high copy number (94 copies) and extremely high levels of over-expression (27-50 fold) developed a significant atrial hypertrophy, dilation and cardiomyopathy. These data indicate that very high expression levels of a contractile protein can cause a cardiac pathology that is unrelated to its degree of replacement in the sarcomere and the unique role(s) it may assume in motor protein 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.