ATP13A2

Protein-coding gene found in humans From Wikipedia, the free encyclopedia

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]

AliasesATP13A2, CLN12, HSA9947, KRPPD, PARK9, ATPase 13A2, SPG78, ATPase cation transporting 13A2
End17,011,928 bp[1]
Quick facts Identifiers, Aliases ...
ATP13A2
Identifiers
AliasesATP13A2, CLN12, HSA9947, KRPPD, PARK9, ATPase 13A2, SPG78, ATPase cation transporting 13A2
External IDsOMIM: 610513; MGI: 1922022; HomoloGene: 56940; GeneCards: ATP13A2; OMA:ATP13A2 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001141973
NM_001141974
NM_022089

RefSeq (protein)

NP_001135445
NP_001135446
NP_071372
NP_001135445.1
NP_001135446.1

Location (UCSC)Chr 1: 16.99 – 17.01 MbChr 4: 140.71 – 140.73 Mb
PubMed search[3][4]
Wikidata
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Deficiency is associated with spastic paraplegia and Kufor-Rakeb syndrome, in which there is progressive parkinsonism with dementia.[14]

References

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