Abstract: Copper is a versatile divalent metal needed as a cofactor for numerous metalloenzymes but can also induce toxic oxidative stress, for which reason its levels are tightly regulated. Multiple gene products maintain copper homeostasis in various cell types. Copper importers, such as copper transporter 1 (CTR1), are responsible for copper uptake into the cytoplasm of cells. In the intracellular milieu, copper chaperones escort the metal ion to designated cellular compartments and other copper transporters. Cytosolic proteins such as metallothioneins bind Cu+ and act as buffers to prevent the production of toxic reactive oxygen species. Finally, the copper transporters ATP7A and ATP7B have dual major functions dictated by intracellular copper levels. In normal copper states, they pump copper into the secretory pathway for metalation of cuproenzymes. When faced with excessive intracellular copper levels, they traffic to the plasma membrane and remove copper from the cell.
Publication Year: 2019
Publication Date: 2019-01-01
Language: en
Type: book-chapter
Indexed In: ['crossref']
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Cited By Count: 3
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