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1 that overexpress a mutated form of the human amyloid-beta precursor protein.
2 rocessing of both the Notch receptor and the amyloid-beta precursor protein.
3 nal cell lines engineered to overexpress the amyloid-beta precursor protein.
4 myloid precursor protein (APP), better named amyloid-beta precursor protein (A(beta)PP), by secretase
5 e core genes were connected to APP (encoding amyloid beta precursor protein), a major player in Alzhe
6 cessing of the familial disease gene product amyloid beta precursor protein (AbetaPP) by beta- and ga
7 brain show alterations in the processing of amyloid beta precursor protein (AbetaPP), including incr
8 Transgenic mice expressing mutant forms of amyloid-beta precursor protein (AbetaPP) and presenilin-
11 the overexpression of a mutated cDNA of the amyloid-beta precursor protein (AbetaPP) or by knock-in
12 muscle fibers we also studied the effect of amyloid-beta precursor protein (AbetaPP) overexpression
13 orms of Alzheimer's disease (AD) encodes the amyloid-beta precursor protein (AbetaPP) substitution mu
14 ysical interaction of the ER chaperones with amyloid-beta precursor protein (AbetaPP) was studied by
17 NCT and PS1 play important roles in binding amyloid beta precursor proteins and modulating PS1 catal
18 se-associated amyloid-beta peptides from the amyloid-beta precursor protein and in releasing the tran
20 ich coexpress mutated human presenilin 1 and amyloid-beta precursor protein) and 30 wild-type mice ag
21 protein expression, that Histone 1 Family 2, amyloid beta precursor protein, and E-cadherin are usefu
22 ntified a caspase-3 cleavage site within the amyloid-beta precursor protein, and a caspase-3 cleavage
23 increased transcription and accumulation of amyloid-beta precursor protein, and accumulation of its
24 a is generated by sequential cleavage of the amyloid beta precursor protein (APP) by beta- and gamma-
26 cts of mutations in the BRI2 (ITM2b) and the amyloid beta precursor protein (APP) genes support the h
27 he familial Alzheimer's disease gene product amyloid beta precursor protein (APP) is sequentially pro
30 iP) that catalyzes the final cleavage of the amyloid beta precursor protein (APP) to release the amyl
31 human form of one of these candidate genes, amyloid beta precursor protein (APP), displayed enhanced
32 dependent C-terminal cleavage product of the amyloid beta precursor protein (APP), Fe65, and Tip60, i
33 essed the effects of isoflurane on beta-site amyloid beta precursor protein (APP)-cleaving enzyme (BA
35 hen tartrate (Posiphen), lowers secreted (s) amyloid-beta precursor protein (APP) alpha and -beta, am
36 s to a significant decrease in intracellular amyloid-beta precursor protein (APP) and extracellular A
39 nic (Tg) mice overexpressing mutant forms of amyloid-beta precursor protein (APP) and presenilin 1 (P
40 three Mints bind to the cytoplasmic tail of amyloid-beta precursor protein (APP) and presenilins and
42 al cell cultures secrete exosomes containing amyloid-beta precursor protein (APP) and the APP-process
44 P-1, which in turn enhances transcription of amyloid-beta precursor protein (APP) and thereby increas
46 ghboring cells that express normal levels of amyloid-beta precursor protein (APP) but show redistribu
49 stigate the production of Abeta11-40/42 from amyloid-beta precursor protein (APP) by beta-site APP-cl
54 al to the gamma-secretase proteolysis of the amyloid-beta precursor protein (APP) involved in Alzheim
57 required for the penultimate cleavage of the amyloid-beta precursor protein (APP) leading to the gene
58 5LO did not induce any significant change in amyloid-beta precursor protein (APP) levels and processi
60 loidogenic amyloid-beta peptide (Abeta) from amyloid-beta precursor protein (APP) requires cleavage b
61 le in Alzheimer disease, is derived from the amyloid-beta precursor protein (APP) through consecutive
62 and inhibits cerebral amyloid deposition in amyloid-beta precursor protein (APP) transgenic mice.
63 re we use Tg2576 mice, which express a human amyloid-beta precursor protein (APP) variant linked to A
64 ng synaptophysin, neurofilament H (NF-H) and amyloid-beta precursor protein (APP) were performed to e
65 n human and mouse leads to downregulation of amyloid-beta precursor protein (APP), a known neuronal m
69 uce any change in the steady state levels of amyloid-beta precursor protein (APP), BACE1 or ADAM10.
70 oidogenic fragments (ie, C99 and Abeta) from amyloid-beta precursor protein (APP), crucial factors ca
72 P cleavage enzyme 1 (BACE1) that cleaves the amyloid-beta precursor protein (APP), which is abundant
77 nd in the brains of Alzheimer's patients and amyloid-beta precursor protein (APP)/PS1 transgenic mice
79 FAD has also been linked to mutations in the amyloid beta precursor protein (beta PP), and the presen
81 ch is derived from proteolysis of the larger amyloid-beta precursor protein (betaAPP), seems to be an
82 pregulated in MDA-MB-231) and GREB1, S100A8, amyloid beta precursor protein, claudin 3 and cadherin 1
83 is required for intramembrane proteolysis of amyloid-beta precursor protein, contributing to the path
85 disease, both caused by a duplication of the amyloid-beta precursor protein gene (APP; termed APP(Dp)
86 sport proteins JNK-interacting protein 1 and amyloid beta precursor protein in the brains and spinal
88 siology of Alzheimer disease (AD), including amyloid-beta precursor protein metabolism, Tau phosphory
89 r order Abeta structures but not full-length amyloid-beta precursor protein or C-terminal amyloid-bet
90 , including transgenic mice expressing human amyloid-beta precursor protein, presenilin 1, and tau mu
92 f the Alzheimer's disease hallmark gene APP (amyloid-beta precursor protein) to the beta-site-cleavin
93 expression and secretase-cleaved products of amyloid-beta precursor protein were not affected by sucr
94 basic hypothesis is that over-expression of amyloid-beta precursor protein within aging muscle fiber
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