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- W3146973539 abstract "Rare genetic mutations in the DJ-1 and Parkin genes cause recessive Parkinsonism, however, the rela- tionship between these two genes is not fully elucidated. Current emerging evidence suggests that these genes are involved in mitochondrial homeostasis, and that a defi- ciency in either of these two genes is associated with damages in mitochondrial function and morphology. In this study, we demonstrated that knockdown of DJ-1 expression or the overexpression of the DJ-1 L166P mutation results in a damaged phenotype in mitochondria and a hypersen- sitivity to H2O2-induced cell apoptosis. These phenotypes result from increased levels of endogenous oxidative stress. However, overexpression of wild-type Parkin rescued the phenotypes observed in the mitochondria of DJ-1 knock- down and DJ-1 L166P mutant cells. We also determined that there were differences between the two cell models. Furthermore, both H2O2 treatment and the DJ-1 L166P mutation weakened the interaction between DJ-1 and Par- kin. Taken together, these findings suggested that DJ-1 and Parkin were linked through oxidative stress, and that overexpression of Parkin protects DJ-1 protein-deficient and DJ-1 L166P mutant-expressing cells via inhibition of oxidative stress." @default.
- W3146973539 created "2021-04-13" @default.
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- W3146973539 date "2013-01-01" @default.
- W3146973539 modified "2023-09-27" @default.
- W3146973539 title "Upregulated Parkin expression protects mitochondrial homeostasis in DJ-1 konckdown cells and cells overexpressing the DJ-1 L166P mutation" @default.
- W3146973539 hasPublicationYear "2013" @default.
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