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Gene Ontology Classifications
Parkinson disease (autosomal recessive, juvenile) 2, parkin

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GO curators for mouse genes have assigned the following annotations to the gene product of Park2. (This text reflects annotations as of Tuesday, May 26, 2015.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of September 8, 2008. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The precise function of this gene is unknown; however, the encoded protein is a component of a multiprotein E3 ubiquitin ligase complex that mediates the targeting of substrate proteins for proteasomal degradation. Mutations in this gene are known to cause Parkinson disease and autosomal recessive juvenile Parkinson disease. Alternative splicing of this gene produces multiple transcript variants encoding distinct isoforms. Additional splice variants of this gene have been described but currently lack transcript support. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
  1. Bouman L et al. (2011) Parkin is transcriptionally regulated by ATF4: evidence for an interconnection between mitochondrial stress and ER stress. Cell Death Differ, 18:769-82. (PubMed:21113145)
  2. Ekholm-Reed S et al. (2013) Parkin-dependent degradation of the F-box protein Fbw7beta promotes neuronal survival in response to oxidative stress by stabilizing Mcl-1. Mol Cell Biol, 33:3627-43. (PubMed:23858059)
  3. Goldberg MS et al. (2003) Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons. J Biol Chem, 278:43628-35. (PubMed:12930822)
  4. Gonzalez S et al. (2005) Cannabinoid CB(1) receptors in the basal ganglia and motor response to activation or blockade of these receptors in parkin-null mice. Brain Res, 1046:195-206. (PubMed:15882845)
  5. Hofmeister-Brix A et al. (2013) Identification of the ubiquitin-like domain of midnolin as a new glucokinase interaction partner. J Biol Chem, 288:35824-39. (PubMed:24187134)
  6. Huynh DP et al. (2001) Differential expression and tissue distribution of parkin isoforms during mouse development. Brain Res Dev Brain Res, 130:173-81. (PubMed:11675120)
  7. Imai Y et al. (2003) A product of the human gene adjacent to parkin is a component of Lewy bodies and suppresses Pael receptor-induced cell death. J Biol Chem, 278:51901-10. (PubMed:14532270)
  8. Itier JM et al. (2003) Parkin gene inactivation alters behaviour and dopamine neurotransmission in the mouse. Hum Mol Genet, 12:2277-91. (PubMed:12915482)
  9. Kitao Y et al. (2007) Pael receptor induces death of dopaminergic neurons in the substantia nigra via endoplasmic reticulum stress and dopamine toxicity, which is enhanced under condition of parkin inactivation. Hum Mol Genet, 16:50-60. (PubMed:17116640)
  10. Kuroda Y et al. (2012) Parkin interacts with Klokin1 for mitochondrial import and maintenance of membrane potential. Hum Mol Genet, 21:991-1003. (PubMed:22082830)
  11. Muller-Rischart AK et al. (2013) The E3 ligase parkin maintains mitochondrial integrity by increasing linear ubiquitination of NEMO. Mol Cell, 49:908-21. (PubMed:23453807)
  12. Navarro P et al. (2008) Memory and exploratory impairment in mice that lack the Park-2 gene and that over-express the human FTDP-17 mutant Tau. Behav Brain Res, 189:350-6. (PubMed:18346797)
  13. Palacino JJ et al. (2004) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice. J Biol Chem, 279:18614-22. (PubMed:14985362)
  14. Sato S et al. (2006) 14-3-3eta is a novel regulator of parkin ubiquitin ligase. EMBO J, 25:211-21. (PubMed:16096643)
  15. Shin JH et al. (2011) PARIS (ZNF746) repression of PGC-1alpha contributes to neurodegeneration in Parkinson's disease. Cell, 144:689-702. (PubMed:21376232)
  16. Staropoli JF et al. (2003) Parkin is a component of an SCF-like ubiquitin ligase complex and protects postmitotic neurons from kainate excitotoxicity. Neuron, 37:735-49. (PubMed:12628165)
  17. Trempe JF et al. (2009) SH3 domains from a subset of BAR proteins define a Ubl-binding domain and implicate parkin in synaptic ubiquitination. Mol Cell, 36:1034-47. (PubMed:20064468)
  18. Um JW et al. (2006) Parkin ubiquitinates and promotes the degradation of RanBP2. J Biol Chem, 281:3595-603. (PubMed:16332688)
  19. Van Humbeeck C et al. (2008) Parkin occurs in a stable, non-covalent, approximately 110-kDa complex in brain. Eur J Neurosci, 27:284-93. (PubMed:18190519)
  20. Von Coelln R et al. (2004) Loss of locus coeruleus neurons and reduced startle in parkin null mice. Proc Natl Acad Sci U S A, 101:10744-9. (PubMed:15249681)
  21. Yun J et al. (2014) MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkin. Elife, 3:e01958. (PubMed:24898855)

Go Annotations in Tabular Form (Text View) (GO Graph)

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Gene Ontology Evidence Code Abbreviations:

  EXP Inferred from experiment
  IAS Inferred from ancestral sequence
  IBA Inferred from biological aspect of ancestor
  IBD Inferred from biological aspect of descendant
  IC Inferred by curator
  IDA Inferred from direct assay
  IEA Inferred from electronic annotation
  IGI Inferred from genetic interaction
  IKR Inferred from key residues
  IMP Inferred from mutant phenotype
  IMR Inferred from missing residues
  IPI Inferred from physical interaction
  IRD Inferred from rapid divergence
  ISS Inferred from sequence or structural similarity
  ISO Inferred from sequence orthology
  ISA Inferred from sequence alignment
  ISM Inferred from sequence model
  NAS Non-traceable author statement
  ND No biological data available
  RCA Reviewed computational analysis
  TAS Traceable author statement


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