Copper homeostasis (Homo sapiens)

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Copper is a redox-active transition metal and an essential trace element for life. It is a catalytic cofactor for numerous enzymes involved in critical biological processes (eg. detoxyfication by oxygen free radicals, angiogenesis, pigmentation, peptide hormone production, etc.). However, "free" copper is harmful for cells because can generate ROS that leads to cellular damage. Thus, all organisms and cells maintain a tight control of its uptake, trafficking and export. This process is rather intricate and requires an interplay between numerous biomolecules (proteins, enzymes, metabolites...) that act as copper ions importers (CTR1, CTR2, DMT1, Prp, APP), chaperones (CCS, ATOX1, COX17, COMMD1) and exporters (ATP7A, ATP7B). Copper ions and Cu-indipendent stimuli (hormone, oxygen, phosphorylation and ubiquination) seem to affect localization and expression of Cu-transporters and chaperones. Potential target of copper ions seem to be crucial signaling pathways, such PI3K/Akt, in which copper induces insulin-like effects. Copper dyshomeostasis could be implicated in cancer and a number of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, prion disease and ALS.