Summary
During the process of enlargement of the heart due to overload, a significant reconstitution of the organ including myoctes and intracellular constituents occurs, as well as cellular hypertrophy induced by increased synthesis of cellular components in order to meet an increased demand in work. This adaptational phenomenon can be defined at the molecular level in terms of altered transcription of specific genes.
Cardiac myosin isoforms, through their enzymatic activities, regulate both contractility and energy efficiency for contraction of the muscle. Since analysis of myosin isoforms can provide insight into the process of caridac hypertrophy, we developed monoclonal antibodies specific for two types of cardiac myosin, and characterized these isoforms by an immunofluorescence study. Furthermore, we cloned specific genes encoding the heavy and light chains of these cardiac myosin isoforms from the human cDNA library and demonstrated the regulation of their expression in the overloaded human heart. In this study, we investigated human materials to obtain clinical implications from our observations.
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© 1989 Springer-Verlag Tokyo
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Yazaki, Y., Tsuchimochi, H., Kurabayashi, M., Komuro, I. (1989). Isozymic Changes in Human Cardiac Myosins Due to Overload. In: Hori, M., Suga, H., Baan, J., Yellin, E.L. (eds) Cardiac Mechanics and Function in the Normal and Diseased Heart. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67957-8_7
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DOI: https://doi.org/10.1007/978-4-431-67957-8_7
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-68020-8
Online ISBN: 978-4-431-67957-8
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