ArticleThe Journal of biological chemistry2009
Solution structure of human cardiac troponin C in complex with the green tea polyphenol, (-)-epigallocatechin 3-gallate.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- Desensitization of the Cardiac Troponin Complex by TnI Phosphorylation and Epigallocatechin-3-Gallate.ACS omega · 2026Article
- Exploring contractile protein mechanisms and target medications for cardiomyopathic patients with diastolic dysfunction.Pediatric discovery · 2024Review
- A green tea extract catechin EGCg: Therapeutic potential for pediatric cardiomyopathies.Pediatric discovery · 2023Review
- Polyphenols as potential enhancers of stem cell therapy against neurodegeneration.Neural regeneration research · 2022Review
- Cardiomyocyte Dysfunction in Inherited Cardiomyopathies.International journal of molecular sciences · 2021Review
- A Potent Fluorescent Reversible-Covalent Inhibitor of Cardiac Muscle Contraction.ACS medicinal chemistry letters · 2021Article
- De Novo Missense Mutations inInternational journal of molecular sciences · 2021Article
- Cardiac troponin I R193H mutant interacts with HDAC1 to repress phosphodiesterase 4D expression in cardiomyocytes.Genes & diseases · 2021Article
- Article
- Dipeptidyl Peptidase-4 Is a Target Protein of Epigallocatechin-3-Gallate.BioMed research international · 2020Article
- Green tea extract catechin improves cardiac function in pediatric cardiomyopathy patients with diastolic dysfunction.Journal of biomedical science · 2019Article
- Analysis of Contractile Function of Permeabilized Human Hypertrophic Cardiomyopathy Multicellular Heart Tissue.Frontiers in physiology · 2019Article
- The calcium sensitizer drug MCI-154 binds the structural C-terminal domain of cardiac troponin C.Biochemistry and biophysics reports · 2018Article
- Computational Molecular Docking and X-ray Crystallographic Studies of Catechins in New Drug Design Strategies.Molecules (Basel, Switzerland) · 2018Review
- Hypertrophic cardiomyopathy mutations increase myofilament CaThe Journal of biological chemistry · 2018Article
- Amide hydrogens reveal a temperature-dependent structural transition that enhances site-II CaScientific reports · 2017Article
- Nebivolol Desensitizes Myofilaments of a Hypertrophic Cardiomyopathy Mouse Model.Frontiers in physiology · 2017Article
- Sarcomere neutralization in inherited cardiomyopathy: small-molecule proof-of-concept to correct hyper-Ca2+-sensitive myofilaments.American journal of physiology. Heart and circulatory physiology · 2016Article
- Epigallocatechin-3-Gallate Accelerates Relaxation and CaFrontiers in physiology · 2016Article
- '(De-)sensitization' vs. 'Uncoupling': what drives cardiomyopathies in the thin filament? Reply.Cardiovascular research · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart muscle contraction is regulated by Ca(2+) binding to the thin filament protein troponin C. In cardiovascular disease, the myofilament response to Ca(2+) is often altered. Compounds that rectify this perturbation are of considerable interest as therapeutics. Plant flavonoids have been found to provide protection against a variety of human illnesses such as cancer, infection, and heart disease. (-)-Epigallocatechin gallate (EGCg), the prevalent flavonoid in green tea, modulates force generation in isolated guinea pig hearts (Hotta, Y., Huang, L., Muto, T., Yajima, M., Miyazeki, K., Ishikawa, N., Fukuzawa, Y., Wakida, Y., Tushima, H., Ando, H., and Nonogaki, T. (2006) Eur. J. Pharmacol. 552, 123-130) and in skinned cardiac muscle fibers (Liou, Y. M., Kuo, S. C., and Hsieh, S. R. (2008) Pflugers Arch. 456, 787-800; and Tadano, N., Yumoto, F., Tanokura, M., Ohtsuki, I., and Morimoto, S. (2005) Biophys. J. 88, 314a). In this study we describe the solution structure of the Ca(2+)-saturated C-terminal domain of troponin C in complex with EGCg. Moreover, we show that EGCg forms a ternary complex with the C-terminal domain of troponin C and the anchoring region of troponin I. The structural evidence indicates that the binding site of EGCg on the C-terminal domain of troponin C is in the hydrophobic pocket in the absence of troponin I, akin to EMD 57033. Based on chemical shift mapping, the binding of EGCg to the C-terminal domain of troponin C in the presence of troponin I may be to a new site formed by the troponin C.troponin I complex. This interaction of EGCg with the C-terminal domain of troponin C.troponin I complex has not been shown with other cardiotonic molecules and illustrates the potential mechanism by which EGCg modulates heart contraction.
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