Primary defect in copper transport underlies mottled mutants in the mouse

IF 48.5 1区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

Nature Pub Date : 1974-06-28 DOI:10.1038/249852a0

D. M. HUNT

引用次数: 285

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.

查看原文本刊更多论文

铜转运的初级缺陷是小鼠斑驳突变体的基础

本文的研究结果表明，铜转运的主要缺陷是小鼠斑驳综合征的基础。因此，X 连锁斑驳突变体为研究哺乳动物的铜代谢提供了一个极好的系统。它们还为同样是 X 连锁的遗传性人类铜缺乏症--门克氏症（Menkes kinky hair disease）1,2 提供了一个动物模型。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Nature 综合性期刊-综合性期刊

CiteScore

90.00

自引率

1.20%

发文量

3652

审稿时长

3 months

期刊介绍： Nature is a prestigious international journal that publishes peer-reviewed research in various scientific and technological fields. The selection of articles is based on criteria such as originality, importance, interdisciplinary relevance, timeliness, accessibility, elegance, and surprising conclusions. In addition to showcasing significant scientific advances, Nature delivers rapid, authoritative, insightful news, and interpretation of current and upcoming trends impacting science, scientists, and the broader public. The journal serves a dual purpose: firstly, to promptly share noteworthy scientific advances and foster discussions among scientists, and secondly, to ensure the swift dissemination of scientific results globally, emphasizing their significance for knowledge, culture, and daily life.