Probable cation-transporting ATPase 13A2 is an enzyme that in humans is encoded by the ATP13A2 gene that is involved in the transport of divalent transition metal cations.[5][6][7] It appears to protect cells from manganese[8] and zinc toxicity,[9] possibly by causing cellular efflux and/or lysosomal sequestration; and from iron toxicity, possibly by preserving lysosome integrity against iron-induced lipid peroxidation.[10] However, it potentiates the toxic effects of cadmium and nickel on developing neurites,[11] and of the widely used herbicide paraquat[12] possibly by increasing polyamine uptake.[13]
ATP13A2 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | ATP13A2, CLN12, HSA9947, KRPPD, PARK9, ATPase 13A2, SPG78, ATPase cation transporting 13A2 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 610513 MGI: 1922022 HomoloGene: 56940 GeneCards: ATP13A2 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Deficiency is associated with spastic paraplegia and Kufor-Rakeb syndrome, in which there is progressive parkinsonism with dementia.[14]