Human amyloid precursor protein

Kumar-Singh, S., Dewachter, I., Moechars, D., Lubke, U., De Jonghe, C., et al. (2000) Behavioral disturbances without amyloid deposits in mice overexpressing human amyloid precursor protein with Flemish (A692G) or Dutch (E693Q) mutation. Neurobiol Dis 7, 9-22. 

Peng Y, Lee DY, Jiang L, Ma Z, Schachter SC, Lemere CA (2007) Hupeizine A regulates amyloid precursor protein processing via protein kinase C and mitogen-activated protein kinase pathways in neuroblastoma SK-N-SH cells over-expressing wild type human amyloid precursor protein 695. Neuroscience 150 386-395... 

Sud M, Fahy E, Cotter D, et al. LMSD LIPID MAPS structure database. Nucleic Acids Res. 2007 35 D527-D532. Tajima Y, Ishikawa M, Maekawa K, et al. Lipidomic analysis of brain tissues and plasma in a mouse model expressing mutated human amyloid precursor protein/tau for Alzheimer s disease. Lipids Health Dis. 2013 12 68. Woods AS, Jackson SN. Brain tissue lipidomics direct probing using matrix-assisted laser desorption/ ionization mass spectrometry. AAPS J. 2006 8(2) E391-395. 

Human amyloid precursor protein Proteolytic cleavage by y-secretase 115, 116... 

Saftig, P. Peters, C. von Figura, K. Crawssaerts, K. Van Leuven, F. De Strooper, B. A Myloidogenic Processing of Human Amyloid Precursor Protein in Hippocampal Neurons Devoid of Cathepsin D. J. Biol Chem., 1996. 271, 27241 27244. 

Abe, K., St. George-Hyslop, P.H., Tanzi, R.E., Kogure, K. (1991). Induction of amyloid precursor protein mRNA after heat shock in cultured human lymphoblastoid cells. Neurosci. Lett. 125, 169-171. 

Yoshikai, S., Sasaki, H., Doh-ura, K., Furuya, H., Sakaki, Y. (1990) Genomic organization of the human amyloid beta-protein precursor gene. Gene, 87, 257-263. 

Primary screening interest for the set was the aspartyl protease /3-secretase,51 one of two proteases that cleave the /3-amyloid precursor protein (APP) to produce /3-amyloid peptide (A/3) in the human brain, a key event in the pathogenesis of Alzheimer s disease.52 No biological data have yet been reported. However, representative examples and a full QC distribution taken from a 10% random selection of the final library are shown in Figs. 10 and 11. 

Antigen unmasking on sections of paraffin-embedded tissues can be accomplished by reduction of disulfide bonds by treatment with 2-mercaptoethanol, followed by alkylation with sodium iodoacetate to prevent the bonds from reforming. This method has been used for unmasking a Kunitz protease inhibitory domain epitope of Alzheimer s amyloid precursor protein in human brain (Campbell et al., 1999). Sections are reduced with a mixture of 0.14 M 2-mercaptoethanol in 0.5 M Tris-HCl (pH 8.0) and 1 mM EDTA for 3 hr in the dark at room temperature. After being washed for 3 min in distilled water, the sections are treated with a mixture of 250 mg/ml iodoacetic acid in 0.1 M NaOH, diluted 1 10 in 0.5 M Tris-HCl (pH 8.0) and 1 mM EDTA for 20 min in the dark. 

Campbell, E., Pearson, R. C. A., and Parkinson, D. 1999. Methods to uncover an antibody epitope in the KPI domain of Alzheimer s amyloid precursor protein for immunohistochemistry in human brain. J. Neurosci. Methods 93 133-138. 

Lin, X., Koelsch, G, Wu, S., Downs, D., Dashti, A., Tang, J. Human aspartic protease memapsin 2 cleaves the (3-secretase site of (3-amyloid precursor protein. Proc. Natl. Acad. Sci. USA 2000, 97, 1456-1460. 

Wolf BA, Wertkin AM, Jolly YC, et al. Muscarinic regulation of Alzheimer s disease amyloid precursor protein secretion and amyloid p-protein production in human neuronal NT2N cells. J Biol Chem 1995 270 4916-4922. 

Dineley KT, Xia X, Bui D, Sweatt JD, Zheng H. Accelerated plaque accumulation, associative learning deficits, and up-regulation of alpha 7 nicotinic receptor protein in transgenic mice co-expressing mutant human presenilin 1 and amyloid precursor proteins. J Biol Chem 2002 277 22,768-22,780. 

Trauma-induced axonal injury (TAI)is an important feature of human TBI. Some investigations have reported that moderate hypothermia can also reduce the generation of traumatically induced axonal injury (6,13). In one study, moderate hypothermia (32°C/4 h) initiated 10 min or 25 min after injury significantly reduced the number of abnormally stained axonal profiles (6). A study by Koizumi and Povlishock (13) reported that posttraumatic hypothermia (32°C/1 h) initiated as late as 1 h after trauma significantly reduced the density of amyloid precursor protein (APP) immunoreacti ve damaged axons within the corticospinal tract. Together, these data indicate that posttraumatic hypothermia in two models of TBI provides substantial protection in terms of axonal... 

Beta-amyloid precursor proteins (/i-APPs) are normal components of the human brain and some other tissues. Proteolysis of these, presumably by serine proteases, generates a 39 to 42 amino acid-long peptide, oc-AP. In AD brains, / -AP aggregates into plaque, the hallmark of AD brains. Some of the... 

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