BAIT

ATP13A2

CLN12, HSA9947, KRPPD, PARK9, RP1-37C10.4
ATPase type 13A2
GO Process (2)
GO Function (2)
GO Component (2)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Homo sapiens

Co-localization

Interaction inferred from two proteins that co-localize in the cell by indirect immunofluorescence only when in addition, if one gene is deleted, the other protein becomes mis-localized. Also includes co-dependent association of proteins with promoter DNA in chromatin immunoprecipitation experiments.

Publication

Common pathogenic effects of missense mutations in the P-type ATPase ATP13A2 (PARK9) associated with early-onset parkinsonism.

Podhajska A, Musso A, Trancikova A, Stafa K, Moser R, Sonnay S, Glauser L, Moore DJ

Mutations in the ATP13A2 gene (PARK9) cause autosomal recessive, juvenile-onset Kufor-Rakeb syndrome (KRS), a neurodegenerative disease characterized by parkinsonism. KRS mutations produce truncated forms of ATP13A2 with impaired protein stability resulting in a loss-of-function. Recently, homozygous and heterozygous missense mutations in ATP13A2 have been identified in subjects with early-onset parkinsonism. The mechanism(s) by which missense mutations potentially cause parkinsonism are ... [more]

PLoS ONE Jul. 07, 2012; 7(6);e39942 [Pubmed: 22768177]

Throughput

  • Low Throughput

Additional Notes

  • figure 4.

Curated By

  • BioGRID