Hokkaido University Collection of Scholarly and Academic Papers >
Faculty of Pharmaceutical Sciences >
Peer-reviewed Journal Articles, etc >
Neuroprotective function of DJ-1 in Parkinson's disease.
|Neuroprotective function of DJ-1 in Parkinson's disease.
|Ariga, Hiroyoshi Browse this author →KAKEN DB
|Takahashi-Niki, Kazuko Browse this author →KAKEN DB
|Kato, Izumi Browse this author
|Maita, Hiroshi Browse this author →KAKEN DB
|Niki, Takeshi Browse this author →KAKEN DB
|Iguchi-Ariga, Sanae M M Browse this author →KAKEN DB
|Oxidative medicine and cellular longevity
|Parkinson's disease (PD) is caused by dopaminergic neuronal death in the substantia nigra, resulting in a reduced level of dopamine in the striatum. Oxidative stress and mitochondrial dysfunction are thought to be major causes of neurodegeneration in PD. Although genetic and environmental factors are thought to affect the onset of PD, precise mechanisms at the molecular level have not been elucidated. The DJ-1 gene is a causative gene for familial PD (park7) and also an oncogene. DJ-1 has various functions, including transcriptional regulation, antioxidative stress reaction, and chaperone, protease, and mitochondrial regulation, and its activity is regulated by its oxidative status, especially that of cysteine 106 (C106) of DJ-1. Excess oxidation of DJ-1, which renders DJ-1 inactive, has been observed in patients with sporadic PD and Alzheimer's disease, suggesting that DJ-1 also participates in the onset and pathogenesis of sporadic PD as well as familial PD. DJ-1 is also a stress sensor and its expression is increased upon various stresses, including oxidative stress. In this review, we describe functions of DJ-1 against oxidative stress and possible roles of DJ-1 in the pathogenesis of PD.
|Appears in Collections:
|薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
Submitter: 有賀 寛芳