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Primary defect in copper transport underlies mottled mutants in the mouse

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Abstract

THE results presented here show that a primary defect in copper transport underlies the mottled syndrome in the mouse. The X-linked mottled mutants thus offer an excellent system for the study of mammalian copper metabolism. They also provide an animal model of the inherited human copper deficiency, Menkes kinky hair disease1,2, which is also X-linked.

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HUNT, D. Primary defect in copper transport underlies mottled mutants in the mouse. Nature 249, 852–854 (1974). https://doi.org/10.1038/249852a0

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  • DOI: https://doi.org/10.1038/249852a0

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