PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression - Kim, D.S., Soonchunhyang University, Cheonan, Republic of Korea; Sohn, E.J., Hallym University, Chuncheon, Republic of Korea; Kim, D.W., Hallym University, Chuncheon, Republic of Korea; Kim, Y.N., Hallym University, Chuncheon, Republic of Korea; Eom, S.A., Hallym University, Chuncheon, Republic of Korea; Yoon, G.H., Hallym University, Chuncheon, Republic of Korea; Cho, S.W., University of Ulsan College of Medicine, Seoul, Republic of Korea; Lee, S.H., Hallym University, Chuncheon, Republic of Korea; Hwang, H.S., Hallym University, Chuncheon, Republic of Korea; Cho, Y.S., Hallym University, Chuncheon, Republic of Korea; Park, J.S., Hallym University, Chuncheon, Republic of Korea; Eum, W.S., Hallym University, Chuncheon, Republic of Korea; et al. (BMB reports, 2012)
Keywords: Animals; Apoptosis; bcl-2-Associated X Protein - metabolism; Cell Line; Cell viability; Cysteamine - analogs & derivatives; Cysteamine - pharmacology; Disease Models, Animal; DNA Fragmentation - drug effects; Dopaminergic Neurons - cytology; Dopaminergic Neurons - metabolism; Genetic Vectors - genetics; Genetic Vectors - metabolism; Humans; Mice; MPTP Poisoning; Oxidative Stress - drug effects; Parkinson Disease - metabolism; Parkinson Disease - pathology; Parkinson's disease; PEP-1-p18; Peptides - pharmacology; Protein therapy; Protein transduction; PROTEINAS; PROTEINE; PROTEINS; 화학