[1] Taira T, Saito Y, Niki T, et al. DJ-1 has a role in antioxidative stress to prevent cell death[J]. EMBO Rep, 2004, 5(2): 213-218.[2] Yang W, Chen L, Ding Y, et al. Paraquat induces dopaminergic dysfunction and proteasome impairment in DJ-1-deficient mice[J]. Hum Mol Genet, 2007, 16(23): 2900-2910.[3] Gonzalez-Polo R, Niso-Santano M, Moran J M, et al. Silencing DJ-1 reveals its contribution in paraquat-induced autophagy[J]. J Neurochem, 2009, 109(3): 889-898.[4] Shamoto-Nagai M, Maruyama W, Kato Y, et al. An inhibitor of mitochondrial complex I, rotenone, inactivates proteasome by oxidative modification and induces aggregation of oxidized proteins in SH-SY5Y cells[J]. J Neurosci Res, 2003, 74(4): 589-597.[5] Sindhu K M, Banerjee R, Senthilkumar K S, et al. Rats with unilateral median forebrain bundle, but not striatal or nigral, lesions by the neurotoxins MPP+ or rotenone display differential sensitivity to amphetamine and apomorphine[J]. Pharmacol Biochem Behav, 2006, 84(2): 321-329.[6] Yokota T, Sugawara K, Ito K, et al. Down regulation of DJ-1 enhances cell death by oxidative stress, ER stress, and proteasome inhibition[J]. Biochem Biophys Res Commun, 2003, 312(4): 1342-1348.[7] Sekito A, Koide-Yoshida S, Niki T, et al. DJ-1 interacts with HIPK1 and affects H2O2-induced cell death[J]. Free Radic Res, 2006, 40(2): 155-165.[8] Shendelman S, Jonason A, Martinat C, et al. DJ-1 is a redox-dependent molecular chaperone that inhibits alpha-synuclein aggregate formation[J]. PLoS Biol, 2004, 2(11): e362.[9] Zhou W, Zhu W, Wilson M A, et al. The oxidation state of DJ-1 regulates its chaperone activity toward alpha-synuclein[J]. J Mol Biol, 2006, 356(4): 1036-1048.[10] Gao H, Yang W, Qi Z, et al. DJ-1 protects dopaminergic neurons against rotenone-induced apoptosis by enhancing ERK-dependent mitophagy[J]. J Mol Biol, 2012, 423(2): 232-248.[11] 高丽,蒋腾,张颖冬.自噬在脑缺血损伤中作用的研究进展[J].中国脑血管病杂志,2012,9(7):377-381.[12] Thomas K J, McCoy M K, Blackinton J, et al. DJ-1 acts in parallel to the PINK1/parkin pathway to control mitochondrial function and autophagy[J]. Hum Mol Genet, 2011, 20(1): 40-50.[13] Luo C, Li Y, Wang H, et al. Mitochondrial accumulation under oxidative stress is due to defects in autophagy[J]. J Cell Biochem, 2013, 114(1): 212-219. |