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Gene Review

Park7  -  Parkinson disease (autosomal recessive,...

Mus musculus

Synonyms: DJ-1, Dj1, Parkinson disease protein 7 homolog, Protein DJ-1
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Disease relevance of Park7


Psychiatry related information on Park7


High impact information on Park7

  • Collectively, our findings suggest an essential role for DJ-1 in dopaminergic physiology and D2 receptor-mediated functions [2].
  • Although DJ-1(-/-) mice had normal numbers of dopaminergic neurons in the substantia nigra, evoked dopamine overflow in the striatum was markedly reduced, primarily as a result of increased reuptake [2].
  • Corticostriatal long-term potentiation was normal in medium spiny neurons of DJ-1(-/-) mice, but long-term depression (LTD) was absent [2].
  • DJ-1/PARK7, a cancer- and Parkinson's disease (PD)-associated protein, protects cells from toxic stresses [5].
  • Restoration of DJ-1 expression to DJ-1-/- mice or cells via adenoviral vector delivery mitigated all phenotypes [3].

Chemical compound and disease context of Park7


Biological context of Park7

  • DJ-1 has been identified as a novel oncogene that transforms mouse NIH3T3 cells in cooperation with activated ras [8].
  • Both genomic DNAs comprise 7 exons spanning about 16-24 kb, in which 2-6 exons encode the DJ-1 protein [8].
  • The human DJ-1 gene was mapped at chromosome 1p36.2-p36.3, a region that has been shown to be a hot spot of chromosome abnormalities in several tumor cells [8].
  • These findings suggest that DJ-1 regulates expressions of genes for which functions are thought to be related to cell death or neurodegeneration [9].
  • DJ-1, sharing no significant homology with the sequences so far reported, did not show transactivation activity in the Gal4 recombinant system, but transformed mouse NIH3T3 cells by itself [10].

Anatomical context of Park7

  • Many sporadic PD patients have a defect in mitochondria respiration, and some of the genes that cause PD are mitochondrial-related (e.g., PINK1, Parkin, DJ1) [11].
  • To analyze the promoter of the human DJ-1 gene, a series of deletion constructs of the region upstream of exon 2 were linked to the luciferase gene, and their luciferase activities were measured in human HeLa cells [8].
  • Lipopolysaccharide (LPS) significantly increased the expression of DJ-1/5.8 in murine peritoneal macrophages (Mphi) and a murine macrophage cell line (J774) [12].
  • The DJ-1 gene does not appear to be a significant risk factor for late onset Lewy body disease in this population [4].
  • The high expression of DJ-1 in neuronal and glial cells, that is not confined to a single functional system or any anatomical area, supports the view of a basic physiological role in cell biology [13].

Associations of Park7 with chemical compounds

  • However, DJ-1 overexpression also reduced postsynaptic dopamine receptor responses in normal mice [1].
  • MPTP drastically reduced dopamine to 19% of normal levels and neither DJ-1 nor Parkin protected against MPTP-induced catecholamine loss under these conditions [1].
  • Our results show that Parkin and DJ-1 inhibit dopamine neuron death and enhance amphetamine-induced dopaminergic function in a mouse model of idiopathic PD [1].
  • Diphenylene iodonium, a flavoenzyme inhibitor, blocked the effect of LPS on DJ-1/5.8 expression [12].
  • DJ-1 was first identified as an activated ras-dependent oncogene product and was later also found to be an infertility-related protein affected by sperm toxicants such as ornidazole (OR) and epichlorohydrin [14].
  • Cytoprotective binding of DJ-1 to ASK1 depends on the central redox-sensitive Cys-106 and may be modulated by peripheral cysteine residues [15].

Analytical, diagnostic and therapeutic context of Park7

  • These results warrant further exploration of DJ-1 and Parkin gene therapy for PD, although a better understanding of their effects on behavior and dopamine neurotransmission is required before these proteins can be safely used.Molecular Therapy (2007) 15 4, 698-704. doi:10.1038/ [1].
  • We used gene targeting to generate DJ-1-deficient mice that were viable, fertile, and showed no gross anatomical or neuronal abnormalities [3].
  • However, DJ-1-/- mice showed hypolocomotion when subjected to amphetamine challenge and increased striatal denervation and dopaminergic neuron loss induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine [3].
  • However, animal models are needed to determine whether and how loss of DJ-1 function leads to Parkinson disease [16].
  • Molecular cloning of human and mouse DJ-1 genes and identification of Sp1-dependent activation of the human DJ-1 promoter [8].


  1. DJ-1 and Parkin Modulate Dopamine-dependent Behavior and Inhibit MPTP-induced Nigral Dopamine Neuron Loss in Mice. Paterna, J.C., Leng, A., Weber, E., Feldon, J., Büeler, H. Mol. Ther. (2007) [Pubmed]
  2. Nigrostriatal dopaminergic deficits and hypokinesia caused by inactivation of the familial Parkinsonism-linked gene DJ-1. Goldberg, M.S., Pisani, A., Haburcak, M., Vortherms, T.A., Kitada, T., Costa, C., Tong, Y., Martella, G., Tscherter, A., Martins, A., Bernardi, G., Roth, B.L., Pothos, E.N., Calabresi, P., Shen, J. Neuron (2005) [Pubmed]
  3. Hypersensitivity of DJ-1-deficient mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) and oxidative stress. Kim, R.H., Smith, P.D., Aleyasin, H., Hayley, S., Mount, M.P., Pownall, S., Wakeham, A., You-Ten, A.J., Kalia, S.K., Horne, P., Westaway, D., Lozano, A.M., Anisman, H., Park, D.S., Mak, T.W. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  4. Polymorphism in the human DJ-1 gene is not associated with sporadic dementia with Lewy bodies or Parkinson's disease. Morris, C.M., O'Brien, K.K., Gibson, A.M., Hardy, J.A., Singleton, A.B. Neurosci. Lett. (2003) [Pubmed]
  5. DJ-1, a cancer- and Parkinson's disease-associated protein, stabilizes the antioxidant transcriptional master regulator Nrf2. Clements, C.M., McNally, R.S., Conti, B.J., Mak, T.W., Ting, J.P. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  6. Sensitivity to oxidative stress in DJ-1-deficient dopamine neurons: an ES- derived cell model of primary Parkinsonism. Martinat, C., Shendelman, S., Jonason, A., Leete, T., Beal, M.F., Yang, L., Floss, T., Abeliovich, A. PLoS Biol. (2004) [Pubmed]
  7. DJ-1 has a role in antioxidative stress to prevent cell death. Taira, T., Saito, Y., Niki, T., Iguchi-Ariga, S.M., Takahashi, K., Ariga, H. EMBO Rep. (2004) [Pubmed]
  8. Molecular cloning of human and mouse DJ-1 genes and identification of Sp1-dependent activation of the human DJ-1 promoter. Taira, T., Takahashi, K., Kitagawa, R., Iguchi-Ariga, S.M., Ariga, H. Gene (2001) [Pubmed]
  9. Expression profiles of genes in DJ-1-knockdown and L 166 P DJ-1 mutant cells. Nishinaga, H., Takahashi-Niki, K., Taira, T., Andreadis, A., Iguchi-Ariga, S.M., Ariga, H. Neurosci. Lett. (2005) [Pubmed]
  10. DJ-1, a novel oncogene which transforms mouse NIH3T3 cells in cooperation with ras. Nagakubo, D., Taira, T., Kitaura, H., Ikeda, M., Tamai, K., Iguchi-Ariga, S.M., Ariga, H. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
  11. Mitochondria mass is low in mouse substantia nigra dopamine neurons: Implications for Parkinson's disease. Liang, C.L., Wang, T.T., Luby-Phelps, K., German, D.C. Exp. Neurol. (2007) [Pubmed]
  12. DJ-1 is an indicator for endogenous reactive oxygen species elicited by endotoxin. Mitsumoto, A., Nakagawa, Y. Free Radic. Res. (2001) [Pubmed]
  13. Expression of DJ-1 in the adult mouse CNS. Bader, V., Ran Zhu, X., Lübbert, H., Stichel, C.C. Brain Res. (2005) [Pubmed]
  14. DJ-1, a target protein for an endocrine disrupter, participates in the fertilization in mice. Okada, M., Matsumoto, K., Niki, T., Taira, T., Iguchi-Ariga, S.M., Ariga, H. Biol. Pharm. Bull. (2002) [Pubmed]
  15. Oxidizable residues mediating protein stability and cytoprotective interaction of DJ-1 with apoptosis signal-regulating kinase 1. Waak, J., Weber, S.S., Görner, K., Schall, C., Ichijo, H., Stehle, T., Kahle, P.J. J. Biol. Chem. (2009) [Pubmed]
  16. Age-dependent motor deficits and dopaminergic dysfunction in DJ-1 null mice. Chen, L., Cagniard, B., Mathews, T., Jones, S., Koh, H.C., Ding, Y., Carvey, P.M., Ling, Z., Kang, U.J., Zhuang, X. J. Biol. Chem. (2005) [Pubmed]
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