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Molecular and cellular aspects of copper transport in developing mammals.
J Nutr. 2003 05; 133(5 Suppl 1):1481S-4S.JN

Abstract

Copper is an essential trace element that requires tightly regulated homeostatic mechanisms to ensure adequate supplies without any toxic effects because of the ability of the metal ion to catalyze the formation of free radicals. The Cu-ATPases, ATP7A and ATP7B, play an important role in the physiological regulation of copper. Adequate supplies of copper are particularly important in developing animals, and in humans this is illustrated by mutations of ATP7A that cause the copper deficiency condition Menkes disease, which is fatal in early childhood. In contrast, mutations in ATP7B result in the genetic toxicosis, Wilson disease. We propose that the physiological regulation of copper is accomplished mainly by the intracellular copper-regulated trafficking of the Cu-ATPases. This process allows the overall copper status in the body to be maintained when levels of copper in the diet alter. A study of the defects in mouse models of Menkes and Wilson diseases has demonstrated that both ATPases play an important role in supplying copper to the developing fetus and neonate.

Authors+Show Affiliations

Centre for Cellular and Molecular Biology, School of Biological and Chemical Sciences, Deakin University, Melbourne, Australia. jmercer@deakin.edu.auNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12730448

Citation

Mercer, Julian F B., and Roxana M. Llanos. "Molecular and Cellular Aspects of Copper Transport in Developing Mammals." The Journal of Nutrition, vol. 133, no. 5 Suppl 1, 2003, 1481S-4S.
Mercer JF, Llanos RM. Molecular and cellular aspects of copper transport in developing mammals. J Nutr. 2003;133(5 Suppl 1):1481S-4S.
Mercer, J. F., & Llanos, R. M. (2003). Molecular and cellular aspects of copper transport in developing mammals. The Journal of Nutrition, 133(5 Suppl 1), 1481S-4S. https://doi.org/10.1093/jn/133.5.1481S
Mercer JF, Llanos RM. Molecular and Cellular Aspects of Copper Transport in Developing Mammals. J Nutr. 2003;133(5 Suppl 1):1481S-4S. PubMed PMID: 12730448.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular and cellular aspects of copper transport in developing mammals. AU - Mercer,Julian F B, AU - Llanos,Roxana M, PY - 2003/5/6/pubmed PY - 2003/6/13/medline PY - 2003/5/6/entrez SP - 1481S EP - 4S JF - The Journal of nutrition JO - J. Nutr. VL - 133 IS - 5 Suppl 1 N2 - Copper is an essential trace element that requires tightly regulated homeostatic mechanisms to ensure adequate supplies without any toxic effects because of the ability of the metal ion to catalyze the formation of free radicals. The Cu-ATPases, ATP7A and ATP7B, play an important role in the physiological regulation of copper. Adequate supplies of copper are particularly important in developing animals, and in humans this is illustrated by mutations of ATP7A that cause the copper deficiency condition Menkes disease, which is fatal in early childhood. In contrast, mutations in ATP7B result in the genetic toxicosis, Wilson disease. We propose that the physiological regulation of copper is accomplished mainly by the intracellular copper-regulated trafficking of the Cu-ATPases. This process allows the overall copper status in the body to be maintained when levels of copper in the diet alter. A study of the defects in mouse models of Menkes and Wilson diseases has demonstrated that both ATPases play an important role in supplying copper to the developing fetus and neonate. SN - 0022-3166 UR - https://www.unboundmedicine.com/medline/citation/12730448/Molecular_and_cellular_aspects_of_copper_transport_in_developing_mammals_ L2 - https://academic.oup.com/jn/article-lookup/doi/10.1093/jn/133.5.1481S DB - PRIME DP - Unbound Medicine ER -