Expression profiles of genes in DJ-1-knockdown and L 166 P DJ-1 mutant cells
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Authors
Nishinaga, HiromiTakahashi-Niki, Kazuko
Taira, Takahiro
Andreadis, Athena
Iguchi-Ariga, Sanai M. M.
Ariga, Hiroyoshi
UMass Chan Affiliations
Department of Cell BiologyDocument Type
Journal ArticlePublication Date
2005-08-24Keywords
Amino Acid SubstitutionAnimals
Gene Expression Regulation
Gene Silencing
Mice
Mutation
NIH 3T3 Cells
Oncogene Proteins
Structure-Activity Relationship
Superoxide Dismutase
tau Proteins
Cell Biology
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Show full item recordAbstract
DJ-1 is a novel oncogene and a causative gene for the familial form of Parkinson's disease (PD). DJ-1 has been shown to play roles in anti-oxidative stress by eliminating reactive oxygen species and in transcriptional regulation of genes. Loss of these functions of DJ-1 is thought to trigger the onset of PD. In this study, to identify genes for which expressions are regulated by DJ-1, DNA microarray analyses were carried out using two mouse NIH3T3 cell lines, DJ-1-knockdown cells and cells harboring an exogenously added L 166 P DJ-1 mutant found in PD patients. In both cell lines, drastic changes in expressions of genes, including genes related to stress, apoptosis, oxidative stress and neurotoxicity, were observed and changes in expressions were confirmed by RT-PCR. Of the genes identified, expression level of the extracellular superoxide dismutase (SOD 3) gene was found to decrease in DJ-1-knockdown cells, while expressions of SOD 1 and SOD 2 genes did not change. Furthermore, expression of the tau gene, a gene whose product gives cells neurotoxicity by aggregation, was found to increase at its promoter level in L 166 P DJ-1 cells. These findings suggest that DJ-1 regulates expressions of genes for which functions are thought to be related to cell death or neurodegeneration.Source
Neurosci Lett. 2005 Dec 16;390(1):54-9. Link to article on publisher's siteDOI
10.1016/j.neulet.2005.07.053Permanent Link to this Item
http://hdl.handle.net/20.500.14038/25675PubMed ID
16115732Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.neulet.2005.07.053