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Copper is an essential trace metal that is required for the catalysis of several important cellular enzymes. However, since an excess of copper can also harm cells due to its potential to catalyze the generation of toxic reactive oxygen species, transport of copper and the cellular copper content are tightly regulated. This chapter summarizes the current knowledge on the importance of copper for cellular processes and on the mechanisms involved in cellular copper uptake, storage and export. In addition, we will give an overview on disturbances of copper homeostasis that are characterized by copper overload or copper deficiency or have been connected with neurodegenerative disorders.

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ZIP14 (encoded by the solute carrier 39 family member 14 [SLC39A14] gene) is a manganese (Mn) transporter that is abundantly expressed in the liver and small intestine. Loss-of-function mutations in SLC39A14 cause severe hypermanganesemia. As the liver is regarded as the main regulatory organ involved in Mn homeostasis, impaired hepatic Mn uptake for subsequent biliary excretion has been proposed as the underlying disease mechanism. However, liver-specific Zip14 knock-out (KO)

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