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학술저널
저자정보
Young Ju Lee (부산대학교) Jun Seo Goo (부산대학교) Ji Eun Kim (부산대학교) So Hee Nam (부산대학교) In Sik Hwang (부산대학교) Sun Il Choi (부산대학교) Hye Ryun Lee (부산대학교) Eon Phil Lee (부산대학교) Hae Wook Choi (부산대학교) Hong Sung Kim (부산대학교) Jae Ho Lee (부산대학교) Young Jin Jung (부산대학교) Hak Jin Kim (서울대학교) Dae Youn Hwang (부산대학교)
저널정보
한국실험동물학회 Laboratory Animal Research Laboratory Animal Research Vol.27 No.4
발행연도
2011.12
수록면
293 - 299 (7page)

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Peroxiredoxin I (Prx I) is a member of the peroxiredoxins (Prxs) family, which are antioxidant enzymes that regulate various cellular process via intracellular oxidative signal pathways. In order to investigate the correlation between Prx I and the γ-secretase complex, which causes Alzheimer’s disease (AD), the expression level of Prx I was firstly evaluated in an animal model for AD. NSE/hPen-2 transgenic (Tg) mice, which were used as animal model in this study, showed a high level of Pen-2 expression and accumulation of Aβ-42 peptides in the hippocampus of brain. The expression level of Prx I was significantly higher on the mRNA and protein level in the brain of this model, while not change in Prx VI expression was observed. Furthermore, to verify the effect of Prx I on the γ-secretase components in vitro, the expression level of these components was analyzed in the Prx I transfectants. Of the components of the γ-secretase complex, the expression of PS-2 and Pen-2 was lower in the transfectants overexpressing Prx I compared to the vector transfectants. However, the expression of APP, NCT and APH-1 did not change in Prx I transfectants. Therefore, these results suggested that the expression of Prx I may be induced by the accumulation of Aβ-42 peptides and the overexpression of Prx I in neuroblastoma cells may regulate the expression of γ-secretase components.

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Materials and Methods
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UCI(KEPA) : I410-ECN-0101-2013-510-001228111