ERK1/2 is an endogenous negative regulator of the γ-secretase activity Su-Kyoung Kim * , Hyun-Jung Park * ,† , Hyun Seok Hong * , Eun Joo Baik † , Min Whan Jung † and Inhee Mook-Jung * ,1 * Department of Biochemistry and Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea; and † Neuroscience program, Ajou University, Suwon, Korea 1 Correspondence: Department of Biochemistry and Cancer Research Institute, Seoul National University College of Medicine, 28 Yungun-dong, Jongro-gu Seoul, 110-799, Korea. E-mail: inhee@snu.ac.kr <h3>SPECIFIC AIMS</h3> Although much progress has been made in identifying the components of γ-secretase complex, which is believed to play an important role in the pathogenesis of Alzheimer’s disease, the endogenous regulatory mechanism of γ-secretase is currently unknown. This study was undertaken to examine the possibility that MEK1/2-ERK1/2 kinase pathways are involved in regulating γ-secretase activity. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Enhancement of γ-secretase activity by MEK1/2 inhibitors</h3> We found that γ-secretase was stimulated by an MEK1/2 inhibitor, but not by a p38 or a JNK inhibitor. Treatment of MEK1/2 specific inhibitors, PD98059 or U0126, dramatically increased γ-secretase activity in ANPP cells as well as primary cortical cultured cells, as assessed by an in vitro
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ERK1/2 is an endogenous negative regulator of the γ-secretase activity
Kim, Su-Kyoung; Park, Hyun-Jung; Hong, Hyun Seok; Baik, Eun Joo; Jung, Min Whan; Mook-Jung, Inhee
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, Volume 20 (1): 157
Fed of American Socs for Experimental Biology – Jan 1, 2006
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