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The molecular basis of copper homeostasis copper-related disorders.
DNA Cell Biol. 2002 Apr; 21(4):259-70.DC

Abstract

Copper is an essential trace element that can be extremely toxic in excess due to the pro-oxidant activity of copper ions. Inherited disorders of copper transport, Menkes disease (copper deficiency), and Wilson disease (copper toxicosis) are caused by mutations of two closely related Cu transporting-ATPases, and demonstrate the essentiality and potential toxicity of copper. Other copper toxicosis conditions in humans and animals have been described, but are not well understood at a molecular level. Copper homeostatic mechanisms are being discovered. One such mechanism is copper-induced trafficking of the Cu-ATPases, which allows cells to provide copper to secreted cupro-proteins but also to efflux excess copper. Oxidative damage induced by copper may be involved in the pathogenesis of neurodegenerative conditions such as Alzheimer's disease, familial amyotrophic lateral sclerosis, and prion diseases.

Authors+Show Affiliations

Centre for Cellular and Molecular Biology, School of Biological and Chemical Sciences, Deakin University, Melbourne, Australia.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12042066

Citation

Llanos, Roxana M., and Julian F B. Mercer. "The Molecular Basis of Copper Homeostasis Copper-related Disorders." DNA and Cell Biology, vol. 21, no. 4, 2002, pp. 259-70.
Llanos RM, Mercer JF. The molecular basis of copper homeostasis copper-related disorders. DNA Cell Biol. 2002;21(4):259-70.
Llanos, R. M., & Mercer, J. F. (2002). The molecular basis of copper homeostasis copper-related disorders. DNA and Cell Biology, 21(4), 259-70.
Llanos RM, Mercer JF. The Molecular Basis of Copper Homeostasis Copper-related Disorders. DNA Cell Biol. 2002;21(4):259-70. PubMed PMID: 12042066.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The molecular basis of copper homeostasis copper-related disorders. AU - Llanos,Roxana M, AU - Mercer,Julian F B, PY - 2002/6/4/pubmed PY - 2002/6/12/medline PY - 2002/6/4/entrez SP - 259 EP - 70 JF - DNA and cell biology JO - DNA Cell Biol. VL - 21 IS - 4 N2 - Copper is an essential trace element that can be extremely toxic in excess due to the pro-oxidant activity of copper ions. Inherited disorders of copper transport, Menkes disease (copper deficiency), and Wilson disease (copper toxicosis) are caused by mutations of two closely related Cu transporting-ATPases, and demonstrate the essentiality and potential toxicity of copper. Other copper toxicosis conditions in humans and animals have been described, but are not well understood at a molecular level. Copper homeostatic mechanisms are being discovered. One such mechanism is copper-induced trafficking of the Cu-ATPases, which allows cells to provide copper to secreted cupro-proteins but also to efflux excess copper. Oxidative damage induced by copper may be involved in the pathogenesis of neurodegenerative conditions such as Alzheimer's disease, familial amyotrophic lateral sclerosis, and prion diseases. SN - 1044-5498 UR - https://www.unboundmedicine.com/medline/citation/12042066/The_molecular_basis_of_copper_homeostasis_copper_related_disorders_ L2 - https://www.liebertpub.com/doi/full/10.1089/104454902753759681?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -