Research Interests The Yu Lab is interested in the molecular and cellular basis of Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia, and related neurodegenerative disorders. Using both in vitro and in vivo approaches, the lab focuses on taking apart and putting together several disease-associated molecular machines, particularly the gamma-secretase complex. It is hoped that by doing so the underlying biological principles of these molecular machines and their relevance to disease pathogenesis will be understood. Biosketch Gang G. Yu, PhD, earned his Ph.D. in Biochemistry and Molecular Biology (1992-1996) from the University of Calgary, Canada. He served as a Postdoctoral Fellow (1996-2001) in the Center for Research into Neurodegenerative Diseases at the University of Toronto, Canada. Dr. Yu joined UT Southwestern in October 2001. Read the Yu Lab diversity statement. Publications Dries DR and Yu G (2008). Assembly, maturation, and trafficking of the gamma-secretase complex in Alzheimer’s disease.” Curr. Alz. Res. 5, 124-138. Sephton C and Yu G (2008). Abeta predictor of Alzheimer’s disease symptoms. Archives of Neurology, 65, 875-876. Tu H, Nelson O, Bezprozvanny A, Wang Z, Lee SF, Hao YH, Serneels L, De Strooper B, Yu G, Bezprozvanny I (2006). Presenilins Form ER Ca(2 ) Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations. Cell 126, 981-993.1. Shah S and Yu G (2006). SorLA: Sorting Out APP. Mol. Interv. 6, 74-76. Shah S, Lee S, Tabuchi K, Hao Y, Yu C, LaPlant Q, Ball H, Dann C, Sudhof T, and Yu G (2005). Nicastrin Functions As A Gamma-Secretase-Substrate Receptor. Cell 122, 435-447. Lee SF, Shah S, Yu C, Wigley WC, Li H, Lim M, Pedersen K, Han W, Thomas P, Lundkvist J, Hao YH, and Yu G (2004). A Conserved GXXXG Motif in APH-1 Is Critical for Assembly and Activity of the Gamma-Secretase Complex. J. Biol. Chem. 279, 4144-4152. Luo W, Wang H, Li H, Kim B, Shah S, Lee HJ, Thinakaran G, Kim TW, Yu G, Xu H (2003). PEN-2 and APH-1 Coordinately Regulate Proteolytic Processing of Presenilin 1. J. Biol. Chem. 278, 7850-7854. Rozmahel R, Mount HT, Chen F, Nguyen V, Huang J, Erdebil S, Liauw J, Yu G, Hasegawa H, Gu Y, Song YQ, Schmidt SD, Nixon RA, Mathews PM, Bergeron C, Fraser P, Westaway D, St. George-Hyslop P (2002). Alleles at the Nicastrin locus modify presenilin 1-deficiency phenotype. Proc Natl Acad Sci U S A. 99, 14452-144527. Yang D, Tandon A, Chen F, Yu G, Yu H, Arawaka S, Hasegawa H, Duthie M, Schmidt S, Nixon R, Ramabhadran T, Mathews P, Gandy S, Mount H, St George-Hyslop P, Fraser P (2002). Mature glycosylation and trafficking of nicastrin modulate its binding to presenilins. J. Biol. Chem. 277, 28135-28142. Lee S, Shah S, Li H, Yu C, Han W, Yu G (2002). Mammalian APH-1 Interacts with Presenilin and Nicastrin and Is Required for Intramembrane Proteolysis of Amyloid-beta Precursor Protein and Notch. J. Biol. Chem. 277, 45013-45019.