DGIST 보도자료-DGIST, 계명대학교와 교류활동 시작(0221).hwp

2012. 02. 21() 053-785-1135, 010-2639-0727, fax 053-785-1109 [] 053-785-1130, 010-6408-1130 DGIST, 22 IT DGIST(, ) 21 . DGIST 8 IT (2 14), (2 21), IT (2 22) 160 . IT , . , , . DGIST DGIST .

2024-02-28

[DGIST 보도자료] DGIST, 계명대학교와 MOU 체결(2013.09.24).hwp

2013.09.24() 053-785-1132, 010-4051-3190, fax 053-785-1109 [] 053-785-1130, 010-6408-1130 DGIST, MOU - - DGIST(, ) 24 1 (MOU) . , , , , . DGIST . , . DGIST DGIST . . , DGIST 2004 , 2009 , 2012 .

2024-02-28

0317 미국텍사스A&M대학교_MOU체결.hwp

2011. 03. 17() 053-785-1130, 011-508-8646, fax 053-785-1109 [ ] 053-785-6400, 010-8570-5434 Texas A&M MOU - - (, ) Texas A&M - . Texas A&M (EEI) 17 11, (MOU) . , , , , . Texas A&M 80 500 , 100 . Oil to Wind 1 (Vestas) . , Texas A&M , (Jerald A. Caton) . (UC Berkeley) , 1980 (MIT) , 40 . : 1. Texas A&M 1 2. EEI(Energy Engineering Institute) 1 3. 1 . 1. Texas A&M 11 , 8 A&M . 2010 , , , , , , , , , 10 150 , 240 . - 2006, Texas A&M . . - . 2001 12 CC' . 6 (, , , , , ) . (GMT) . , , 2018 . - , Oil to Wind" 1 Vestas . Texas A&M 80 500 . 100 . 2. EEI(Energy Engineering Institute, ) Texas A&M , . . Oil to Wind" 1 Vestas . . . ( : Solar, Wind, Electric Power, Energy Efficiency, Oil & Gas, Bioenergy, Geothermal, Nuclear) 3. (Jerald A. Caton) : Caton : Jerald 1973 (Honor Student) 1980 (MIT) 1985 - A&M 1987 - 1994 1991 - 1992 1992 - 1994, 1996 - 1997 American Men and Women of Science 2005 - 2009 - A&M Search Committee 2008 A&M 1990 Ralph Teetor

2024-02-28

성균관대학교_정성권_교수_세미나_자료.pptx

Molecular mechanism for Alzheimers disease: possible therapeutic targets Sungkwon Chung, Ph. D. Dept. of Physiology, Sungkyunkwan University, School of Medicine 13:30-14:30, April 4, Wednesday, 2012 Room 103, Building 1, DGIST Familial Alzheimers disease (FAD)-associated mutations in genes encoding presenilin 1 or 2 (PS1, PS2) lead to several cellular phenotypes, including alteration in -secretase-mediated cleavage of -amyloid precursor protein (APP) which liberates amyloid -peptide (A), leading to increase in amyloidogenic 42-residue A (A42) relative to A40. Independent of their role in -secretase function, presenilins are shown to modulate Ca2+ entry. We found that Ca2+ entry via the transient receptor potential melastatin 7 (TRPM7) channel was attenuated by the presence of FAD-associated PS1 mutants, such as E9 and L286V. Since our previous studies showed that the down-regulation of phosphatidylinositol-4,5-bisphosphate (PIP2) is attributable to the observed Ca2+ deficits, we attempted to test whether the intracellular delivery of PIP2 could restore theses phenotypes from FAD-associated PS mutants. Also, application of PIP2 reduced A42 levels but not A40 levels from PS mutant-transfected cells. Interestingly, A42 levels were not changed by PIP2 from PS wild-type cells, indicating that the effect of intracellular PIP2 is specific for PS mutant. Thus, the down-regulated PIP2 level may play an important role for regulating Ca2+ influx as well as the increased generation of A42 from FAD-associated PS mutants. Our results also indicate that regulating intracellular PIP2 level is a potential therapeutic target for AD. O-GlcNAcylation is a novel type of O-linked glycosylation attaching the monosaccharide N-acetylglucosamine (GlcNAc) to serine and threonine residues. In fact, APP was the first plasma membrane protein shown to be O-GlcNAcylated. Recently, it is shown that O-GlcNAcylation of APP increases the non-amyloidogenic processing of APP and decreases the production of A. Even though O-GlcNAcylation has been shown to modify the processing of APP, the role of O-GlcNAcylation in APP trafficking and endocytosis remains unknown. We found that when O-GlcNAcylated APP was increased, the level of APP in the plasma membrane was increased. Also, the level of sAPP (-secretase product) increased, while the level of sAPPb(b-secretase product) was concomitantly decreased, indicating the increased non-amyloidogenic processing of APP. Consistent with this results, the secreted levels of A species (A40 and A42) decreased. These results strongly indicate that O-GlcNAcylation increases the plasma membrane targeting of APP, where it can be cleaved preferentially by -secretase and g-secretase. The non-amyloidogenic processing of APP reduces the generation of A. Thus, O-GlcNAcylation of APP is implied as a potential therapeutic target for AD. ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- Person in charge : Jeong Min Lee, Contact: yjm0329@dgist.ac.kr, 053)785-6101 Seminar Department of Brain Science

2024-02-28