New Modes of GPCR Signalling

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β-Secretase (BACE1). Biological Medicinal Chemistry Letters, 19(1): 264-74. 9. Ewers, M., Zhong, Z., Teipel, S., Büger, K., Wallin, A., Blennow, K., and Shen, Y*. and Hampel, H*.(2008). Increased CSF-BACE1 activity is associated with ApoE-ε4 genotype in subjects with mild cognitive impairment and Alzheimer’s disease, Brain, 131:1252-8. 10. Zhong, Z., Ewers, M., Teipel, S., Büger, K., Wallin, A., Blennow, K., Hampel, H., and Shen, Y. (2007). High Levels of Beta-Secretase (BACE1) in Cerebrospinal Fluid as a Predictor of Risk in Mild Cognitive Impairment, the early stage of Alzheimer ’s disease, Archive of General Psychiatry, 64(6):718-26. 11. He P, Zhong Z, Lindholm K, Berning L, Lee W, Lemere C, Staufenbiel M, Li R and ShenY. (2007). Deletion of TNF death receptor inhibits amyloid beta generation and prevents learning and memory deficits in Alzheimer’s mice. Journal of Cell Biology, 178(5): 829-841. Highlighted as “Death receptor takes central stage” by Nature Neuroscience,October, 2007; Hot story by Science, 2007. 12. Tesco G, Koh YH, Kang EL, Cameron AN, Das S, Sena-Esteves M, Hiltunen M, Yang SH, Zhong Z, Shen Y, Simpkins JW, Tanzi RE. (2007). Depletion of GGA3 stabilizes BACE and enhances beta-secretase activity. Neuron.54(5):721-37. 13. Kim DY, Carey BW, Wang H, Ingano LA, Binshtok AM, Wertz MH, Pettingell WH, He P, Lee VM, Woolf CJ, Kovacs DM. (2007). BACE1 regulates voltage-gated sodium channels and neuronal activity. Nature Cell Biol. 9(7):755-64. 14. Yue X, Lu M, Lancaster T, Cao P, Honda S, Staufenbiel M, Harada N, Zhong Z, Shen Y, Li R. (2005). Brain estrogen deficiency accelerates Abeta plaque formation in an Alzheimer's disease animal model. Proc Natl Acad Sci U S A. 102(52):19198-203. 15. Li R., Yang LB, Lindholm K, Yan R, Citron M, Beach T, Sue L, Subbagh M., Cai H., Wong P, Price D, Shen Y.(2004). Aβ load is correlated with elevated BACE activity in sporadic Alzheimer patients. Proc Natl Acad Sci U S A.),101(10), 3632-3637. 16. Li R., Lindholm K, Yang LB, Konishi Y, Hampel H, Zhang, D. Shen Y. (2004). TNF death receptor signaling cascade is required for amyloid-β-protein induced neuron death. J.Neurosci, 28(7), 1760-1771. 17. Yang LB, Lindholm K, Yan R, Citron M, Xia W, Beach T, Sue L, Wong P, Price D, Li R, Shen Y. (2003). Elevated beta-secretase expression and enzymatic activity detected in sporadic Alzheimer disease. Nature.Med, 9(1): 3-4 18. Yang, L-B., Lindholm, K., Konishi, Y., Li, R. and Shen, Y. (2002) Targeting deletion of TNF receptor subtypes reveals hippocampal neuron survival and death through distinct signal transduction pathways. J.Neurosci, 22(8), 3025-3032. 19. Yang, L-B., Li, R., Meri, S., Rogers, J. and Shen, Y. (2000) Deficiency of complement protective protein, CD59 in Alzheimer’s brains may contribute to neurodegeneration. J.Neurosci, 20(20), 7505-7509.
ABSTRACT From Bench to Bedside: BACE1, the Beta-Secretase Enzyme, in Basic Science and Clinical Investigation Yong Shen Robert Haldeman Laboratory of Molecular and Cellular Neurobiology Banner Sun Health Research Institute β-Secretase, or β-site amyloid precursor protein cleaving enzyme 1 (BACE1), has been identified as the rate-limiting enzyme for amyloid-beta (Aβ) peptide production that occurs primarily in neurons in the brain. Aβis the main component of amyloid plaques and vascular deposits in Alzheimer's disease (AD) brains, and it is believed to initiate the deadly amyloid cascade that leads to neurodegeneration and dementia. BACE1 is the principle beta-secretase, as its knock-out completely prevents Aβ generation. BACE1 is likely to process a number of different substrates, and consequently, it may exert several independent physiological functions in neurons. Currently, however, the physiological functions of BACE1 are not clear. Multiple cellular mechanisms for BACE1 regulation, including transcriptional regulation, neuronal excitability, receptor mediation, and identification of new molecules as biomarkers for AD and molecular targeting for Aβ lowering therapies will be discussed.
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