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DJ‐1 has a role in antioxidative stress to prevent cell death
Author(s) -
Taira Takahiro,
Saito Yoshiro,
Niki Takeshi,
IguchiAriga Sanae M M,
Takahashi Kazuhiko,
Ariga Hiroyoshi
Publication year - 2004
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400074
Subject(s) - programmed cell death , hydrogen peroxide , gene knockdown , mutant , small interfering rna , oxidizing agent , oxidative stress , rna , cell , catalase , in vitro , chemistry , microbiology and biotechnology , mutation , biology , cell culture , biochemistry , genetics , apoptosis , gene , organic chemistry
Deletion and point (L166P) mutations of DJ‐1 have recently been shown to be responsible for the onset of familial Parkinson's disease (PD, PARK7). The aim of this study was to determine the role of DJ‐1 in PD. We first found that DJ‐1 eliminated hydrogen peroxide in vitro by oxidizing itself. We then found that DJ‐1 knockdown by short interfering RNA rendered SH‐SY5Y neuroblastoma cells susceptible to hydrogen peroxide‐, MPP+‐ or 6‐hydroxydopamine‐induced cell death and that cells harbouring mutant forms of DJ‐1, including L166P, became susceptible to death in parallel with the loss of oxidized forms of DJ‐1. These results clearly showed that DJ‐1 has a role in the antioxidative stress reaction and that mutations of DJ‐1 lead to cell death, which is observed in PD.