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Research Article Free access | 10.1172/JCI116844

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

J H Qiao, C L Welch, P Z Xie, M C Fishbein, and A J Lusis

Department of Medicine, University of California, Los Angeles 90024.

Find articles by Qiao, J. in: JCI | PubMed | Google Scholar

Department of Medicine, University of California, Los Angeles 90024.

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Department of Medicine, University of California, Los Angeles 90024.

Find articles by Xie, P. in: JCI | PubMed | Google Scholar

Department of Medicine, University of California, Los Angeles 90024.

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Department of Medicine, University of California, Los Angeles 90024.

Find articles by Lusis, A. in: JCI | PubMed | Google Scholar

Published November 1, 1993 - More info

Published in Volume 92, Issue 5 on November 1, 1993
J Clin Invest. 1993;92(5):2386–2393. https://doi.org/10.1172/JCI116844.
© 1993 The American Society for Clinical Investigation
Published November 1, 1993 - Version history
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Abstract

Lipofuscin pigment, a terminal oxidation product, accumulates within cells during the normal aging process and under certain pathological conditions. We have analyzed a genetic cross between two inbred mouse strains, BALB/cJ and a subline of C57BL/6J, which differ in lipofuscin deposition. A comparison of the segregation pattern of cardiac lipofuscin with the albino locus (c) on mouse chromosome 7 revealed complete concordance. Analysis of spontaneous mutants of the tyrosinase gene, encoded by the albino locus, confirmed that the tyrosinase gene itself controls lipofuscin formation. Genetic analysis of other strains indicated that one or more additional genes cab contribute to the inheritance of lipofuscin. We also present evidence for an association between cardiac lipofuscin deposition and aortic fatty streak development in the mouse.

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