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 (e.g. detoxification by oxygen free radicals, angiogenesis, pigmentation, peptide hormone production, etc.). However, "free" copper is harmful for cells because it 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 (e.g. proteins, 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-independent stimuli (hormone, oxygen, phosphorylation and ubiquination) seem to affect localization and expression of Cu-transporters and chaperones. Potential targets of copper ions seem to be crucial signaling pathways, such as 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. Proteins on this pathway have targeted assays available via the CPTAC Assay Portal