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Research Article Free access | 10.1172/JCI113627

Molecular cloning and characterization of human cardiac alpha- and beta-form myosin heavy chain complementary DNA clones. Regulation of expression during development and pressure overload in human atrium.

M Kurabayashi, H Tsuchimochi, I Komuro, F Takaku, and Y Yazaki

Third Department of Internal Medicine, University of Tokyo, Japan.

Find articles by Kurabayashi, M. in: PubMed | Google Scholar

Third Department of Internal Medicine, University of Tokyo, Japan.

Find articles by Tsuchimochi, H. in: PubMed | Google Scholar

Third Department of Internal Medicine, University of Tokyo, Japan.

Find articles by Komuro, I. in: PubMed | Google Scholar

Third Department of Internal Medicine, University of Tokyo, Japan.

Find articles by Takaku, F. in: PubMed | Google Scholar

Third Department of Internal Medicine, University of Tokyo, Japan.

Find articles by Yazaki, Y. in: PubMed | Google Scholar

Published August 1, 1988 - More info

Published in Volume 82, Issue 2 on August 1, 1988
J Clin Invest. 1988;82(2):524–531. https://doi.org/10.1172/JCI113627.
© 1988 The American Society for Clinical Investigation
Published August 1, 1988 - Version history
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Abstract

We have constructed and characterized two types of myosin heavy chain (MHC) cDNA clones (pHMHC2, pHMHC5) from a fetal human heart cDNA library. Comparison of the nucleotide and deduced amino acid sequences between pHMHC2 and pHMHC5 shows 95.1 and 96.2% homology, respectively. The carboxyl-terminal peptide and 3'-untranslated (3'-UT) regions are highly divergent and specific for these cDNA clones. By using the synthetic oligonucleotide probes that are complementary to the unique 3'-UT regions of these cDNA clones, we demonstrate that pHMHC2 is exclusively transcribed in the atrium, whereas the mRNA for pHMHC5 is predominantly expressed in the ventricle. This result indicates that pHMHC2 and pHMHC5 code for alpha- and beta-form MHCs, respectively. Furthermore, we show that beta-form MHC mRNA is expressed in adult atrium at a low level but scarcely expressed in fetal atrium. Finally, we demonstrate that MHC isozymic transition in pressure-overloaded atrium is, at least in part, regulated at a pretranslational level.

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