%0 Journal Article
%T PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression
%A Duk-Soo Kim2
%A #
%A Eun Jeong Sohn1
%A #
%A Dae Won Kim1
%A Young Nam Kim1
%A Seon Ae Eom1
%A Ga Hyeon Yoon1
%A Sung-Woo Cho3
%A Sang-Hyun Lee1
%A Hyun Sook Hwang1
%A Yoon Shin Cho1
%A Jinseu Park1
%A Won Sik Eum1
%A * & Soo Young Choi1
%A *
%J BMB Reports
%D 2012
%I Korean Society for Biochemistry and Molecular Biology
%X P18, a member of the INK4 family of cyclin-dependent kinaseinhibitors, is a tumor suppressor protein and plays a key cellsurvival role in a variety of human cancers. Under pathophysiologicalconditions, the INK4 group proteins participate in novelbiological functions associated with neuronal diseases andoxidative stress. Parkinson¡¯s disease (PD) is characterized by loss ofdopaminergic neurons, and oxidative stress is important in itspathogenesis. Therefore, we examined the effects of PEP-1-p18 onoxidative stress-induced SH-SY5Y cells and in a PD mouse model.The transduced PEP-1-p18 markedly inhibited 1-methyl-4-phenylpyridinium-induced SH-SY5Y cell death by inhibiting Baxexpression levels and DNA fragmentation. Additionally, PEP-1-p18prevented dopaminergic neuronal cell death in the substantia nigraof a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced PDmouse model. These results indicate that PEP-1-p18 may be auseful therapeutic agent against various diseases and is a potentialtool for treating PD.
%K Cell viability
%K Parkinson¡¯s disease
%K PEP-1-p18
%K Protein therapy
%K Protein transduction
%U http://www.jbmb.or.kr/jbmb/pdf.php?data=MTMwMTIyMTdAcGRmX3JhaW50cmFjZV9sZWV5c0AlNUI0NS05JTVEMTIwOTI3MTUzOF8lMjg1MzItNTM3JTI5Qk1CXzEyLTA4My5wZGY=