Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Park7. (This text reflects annotations as of Wednesday, January 23, 2013.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of April 4, 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.

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The product of this gene belongs to the peptidase C56 family of proteins. It acts as a positive regulator of androgen receptor-dependent transcription. It may also function as a redox-sensitive chaperone, as a sensor for oxidative stress, and it apparently protects neurons against oxidative stress and cell death. Defects in this gene are the cause of autosomal recessive early-onset Parkinson disease 7. Two transcript variants encoding the same protein have been identified for this gene. [provided by RefSeq, Jul 2008]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Park7
  • participates in the following biological processes:
    • response to hydrogen peroxide ^[6]
  • is located in the following cellular components:
    • mitochondrion ^{[1, 8]}
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Park7
  • participates in the following biological processes:
    • adult locomotory behavior ^{[2, 4]}
    • cellular response to hydrogen peroxide ^[6]
    • cellular response to oxidative stress ^[5]
    • dopamine uptake involved in synaptic transmission ^[4]
    • hydrogen peroxide metabolic process ^[1]
    • membrane depolarization ^[9]
    • membrane hyperpolarization ^[9]
    • mitochondrion organization ^[7]
    • negative regulation of cell death ^[6]
    • oxidation-reduction process ^[1]
    • positive regulation of oxidative phosphorylation uncoupler activity ^[5]
    • protein stabilization ^[3]
    • regulation of inflammatory response ^[10]
    • response to hydrogen peroxide ^[6]
    • response to stress ^[9]
    • synaptic transmission, dopaminergic ^[2]
  • performs the following molecular functions:
    • peroxidase activity ^[1]
    • peroxiredoxin activity ^[1]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Park7:
  • participates in the following biological processes:
    • cellular response to hydrogen peroxide
    • negative regulation of cell death
    • negative regulation of extrinsic apoptotic signaling pathway
    • negative regulation of neuron apoptotic process
    • negative regulation of protein binding
    • protein stabilization
    • regulation of androgen receptor signaling pathway
    • regulation of neuron apoptotic process
    • response to oxidative stress
  • performs the following molecular functions:
    • mRNA binding
    • peptidase activity
    • protein homodimerization activity
  • is located in the following cellular components:
    • axon
    • cytoplasm
    • cytosol
    • mitochondrion
    • nucleus

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Park7 indicates that it:
  • participates in the following biological processes:
    • autophagy
    • inflammatory response
    • proteolysis
    • single fertilization
  • performs the following molecular functions:
    • hydrolase activity

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References

1. Andres-Mateos E et al. (2007) DJ-1 gene deletion reveals that DJ-1 is an atypical peroxiredoxin-like peroxidase. Proc Natl Acad Sci U S A, 104:14807-12. (PubMed:17766438)
2. Chen L et al. (2005) Age-dependent motor deficits and dopaminergic dysfunction in DJ-1 null mice. J Biol Chem, 280:21418-26. (PubMed:15799973)
3. Clements CM et al. (2006) DJ-1, a cancer- and Parkinson's disease-associated protein, stabilizes the antioxidant transcriptional master regulator Nrf2. Proc Natl Acad Sci U S A, 103:15091-6. (PubMed:17015834)
4. Goldberg MS et al. (2005) Nigrostriatal dopaminergic deficits and hypokinesia caused by inactivation of the familial Parkinsonism-linked gene DJ-1. Neuron, 45:489-96. (PubMed:15721235)
5. Guzman JN et al. (2010) Oxidant stress evoked by pacemaking in dopaminergic neurons is attenuated by DJ-1. Nature, 468:696-700. (PubMed:21068725)
6. Kim RH et al. (2005) Hypersensitivity of DJ-1-deficient mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) and oxidative stress. Proc Natl Acad Sci U S A, 102:5215-20. (PubMed:15784737)
7. Krebiehl G et al. (2010) Reduced basal autophagy and impaired mitochondrial dynamics due to loss of Parkinson's disease-associated protein DJ-1. PLoS One, 5:e9367. (PubMed:20186336)
8. Pagliarini DJ et al. (2008) A mitochondrial protein compendium elucidates complex I disease biology. Cell, 134:112-23. (PubMed:18614015)
9. Pisani A et al. (2006) Enhanced sensitivity of DJ-1-deficient dopaminergic neurons to energy metabolism impairment: role of Na+/K+ ATPase. Neurobiol Dis, 23:54-60. (PubMed:16624565)
10. Waak J et al. (2009) Regulation of astrocyte inflammatory responses by the Parkinson's disease-associated gene DJ-1. FASEB J, 23:2478-89. (PubMed:19276172)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

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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