ArticleThe Journal of general physiology2019
The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM.
Article in The Journal of general physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Heterogeneous Dysregulation of Myosin Super-Relaxation and Energetics in Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2025Article
- The highly conserved C-terminal end segment of troponin T binds tropomyosin and actin to function in modulating contractile kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The abnormalities of free fatty acid metabolism in patients with hypertrophic cardiomyopathy, a single-center retrospective observational study.BMC cardiovascular disorders · 2024Observational
- Slower Calcium Handling Balances Faster Cross-Bridge Cycling in HumanCirculation research · 2023Article
- Animal models and animal-free innovations for cardiovascular research: current status and routes to be explored. Consensus document of the ESC Working Group on Myocardial Function and the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2022Article
- Low expression of the K280NJournal of molecular and cellular cardiology plus · 2022Article
- How low can you go - Insight into the level of mutated protein required to cause pathogenic effects in hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2022Article
- Dysfunctional sarcomeric relaxation in the heart.Current opinion in physiology · 2022Article
- Titin-truncating mutations associated with dilated cardiomyopathy alter length-dependent activation and its modulation via phosphorylation.Cardiovascular research · 2022Article
- Distinct Metabolomic Signatures in Preclinical and Obstructive Hypertrophic Cardiomyopathy.Cells · 2021Article
- Mavacamten has a differential impact on force generation in myofibrils from rabbit psoas and human cardiac muscle.The Journal of general physiology · 2021Article
- The relation between sarcomere energetics and the rate of isometric tension relaxation in healthy and diseased cardiac muscle.Journal of muscle research and cell motility · 2021Article
- Force Measurements From Myofibril to Filament.Frontiers in physiology · 2021Review
- Increased Myocardial Oxygen Consumption Precedes Contractile Dysfunction in Hypertrophic Cardiomyopathy Caused by PathogenicJournal of the American Heart Association · 2020Article
- Pressure Overload Is Associated With Low Levels of Troponin I and Myosin Binding Protein C Phosphorylation in the Hearts of Patients With Aortic Stenosis.Frontiers in physiology · 2020Article
- Review
- Protein Quality Control Activation and Microtubule Remodeling in Hypertrophic Cardiomyopathy.Cells · 2019Article
- A step towards understanding the molecular nature of human heart failure: advances using the Sydney Heart Bank collection.Biophysical reviews · 2019Article
- Toward an understanding of the regulation of myofibrillar function.The Journal of general physiology · 2019Article
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Authors and funding
21 authors at 8 institutions in 5 countries.
Funding
Abstract
Hypertrophic cardiomyopathy (HCM) is a genetic form of left ventricular hypertrophy, primarily caused by mutations in sarcomere proteins. The cardiac remodeling that occurs as the disease develops can mask the pathogenic impact of the mutation. Here, to discriminate between mutation-induced and disease-related changes in myofilament function, we investigate the pathogenic mechanisms underlying HCM in a patient carrying a homozygous mutation (K280N) in the cardiac troponin T gene (
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Registered trials
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