| pubmed-article:14749723 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14749723 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:14749723 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:14749723 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:14749723 | lifeskim:mentions | umls-concept:C1424222 | lld:lifeskim |
| pubmed-article:14749723 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:14749723 | pubmed:dateCreated | 2004-1-29 | lld:pubmed |
| pubmed-article:14749723 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:14749723 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14749723 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14749723 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:14749723 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14749723 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:14749723 | pubmed:issn | 1469-221X | lld:pubmed |
| pubmed-article:14749723 | pubmed:author | pubmed-author:ArigaHiroyosh... | lld:pubmed |
| pubmed-article:14749723 | pubmed:author | pubmed-author:SaitoYoshiroY | lld:pubmed |
| pubmed-article:14749723 | pubmed:author | pubmed-author:NikiTakeshiT | lld:pubmed |
| pubmed-article:14749723 | pubmed:author | pubmed-author:TairaTakahiro... | lld:pubmed |
| pubmed-article:14749723 | pubmed:author | pubmed-author:Iguchi-ArigaS... | lld:pubmed |
| pubmed-article:14749723 | pubmed:author | pubmed-author:TakahashiKazu... | lld:pubmed |
| pubmed-article:14749723 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14749723 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:14749723 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14749723 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14749723 | pubmed:pagination | 213-8 | lld:pubmed |
| pubmed-article:14749723 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:14749723 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14749723 | pubmed:articleTitle | DJ-1 has a role in antioxidative stress to prevent cell death. | lld:pubmed |
| pubmed-article:14749723 | pubmed:affiliation | Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Sapporo 060-0812, Japan. | lld:pubmed |
| pubmed-article:14749723 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14749723 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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