ArticleThe Journal of clinical investigation1998
A mouse model of myosin binding protein C human familial hypertrophic cardiomyopathy.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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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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Who cites it
65 citing papers in PubMed, 198 citations in OpenAlex.
- Genetic Animal Models of Cardiovascular Pathologies.Biomedicines · 2025Review
- AAV9-mediated MYBPC3 gene therapy with optimized expression cassette enhances cardiac function and survival in MYBPC3 cardiomyopathy models.Nature communications · 2025Article
- Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024Article
- Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024Article
- Genome Editing and Pathological Cardiac Hypertrophy.Advances in experimental medicine and biology · 2023Article
- Targeting the sarcomere in inherited cardiomyopathies.Nature reviews. Cardiology · 2022Review
- Cardiomyocyte Dysfunction in Inherited Cardiomyopathies.International journal of molecular sciences · 2021Review
- Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.Biomolecules · 2021Review
- The N terminus of myosin-binding protein C extends toward actin filaments in intact cardiac muscle.The Journal of general physiology · 2021Article
- Breakdown of Filamentous Myofibrils by the UPS-Step by Step.Biomolecules · 2021Review
- Allelic imbalance and haploinsufficiency in MYBPC3-linked hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Altered force generation and cell-to-cell contractile imbalance in hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Advanced Evolution of Pathogenesis Concepts in Cardiomyopathies.Journal of clinical medicine · 2019Review
- Recovery of left ventricular function following in vivo reexpression of cardiac myosin binding protein C.The Journal of general physiology · 2019Article
- INDUCED PLURIPOTENT STEM CELLS FOR MODELLING ENERGETIC ALTERATIONS IN HYPERTROPHIC CARDIOMYOPATHY.Conditioning medicine · 2019Article
- Functional significance of HCM mutants of tropomyosin, V95A and D175N, studied withBiophysics and physicobiology · 2019Article
- In vivo definition of cardiac myosin-binding protein C's critical interactions with myosin.Pflugers Archiv : European journal of physiology · 2016Article
- Knockdown of fast skeletal myosin-binding protein C in zebrafish results in a severe skeletal myopathy.The Journal of general physiology · 2016Article
- The genetic basis of hypertrophic cardiomyopathy in cats and humans.Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology · 2015Review
- Animal and in silico models for the study of sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
5 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Familial hypertrophic cardiomyopathy can be caused by mutations in genes encoding sarcomeric proteins, including the cardiac isoform of myosin binding protein C (MyBP-C), and multiple mutations which cause truncated forms of the protein to be made are linked to the disease. We have created transgenic mice in which varying amounts of a mutated MyBP-C, lacking the myosin and titin binding domains, are expressed in the heart. The transgenically encoded, truncated protein is stable but is not incorporated efficiently into the sarcomere. The transgenic muscle fibers showed a leftward shift in the pCa2+-force curve and, importantly, their power output was reduced. Additionally, expression of the mutant protein leads to decreased levels of endogenous MyBP-C, resulting in a striking pattern of sarcomere disorganization and dysgenesis.
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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.