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1 and the soluble fraction beta of the amyloid precursor protein).
2 n presenilin 1, presenilin 2, or the amyloid precursor protein.
3 phosphorylated tau 181, and soluble amyloid precursor protein.
4 secretase of the Alzheimer's disease amyloid precursor protein.
5 ration in neurons overexpressing human Abeta-precursor protein.
6 proteolytic activation of the dimerized BMP7 precursor protein.
7 reased proteolytic processing of the amyloid precursor protein.
8 related processes and degradation of amyloid precursor proteins.
9 ocessing peptidase for complex mitochondrial precursor proteins.
10 of plant life and are usually synthesized as precursor proteins.
11 ochondria requires the import of hundreds of precursor proteins.
12 es can lead to the accumulation of cytosolic precursor proteins.
13 0)/HSP90-mediated transport of mitochondrial precursor proteins.
14 were connected to APP (encoding amyloid beta precursor protein), a major player in Alzheimer's diseas
15 oxycycline (dox) to suppress further amyloid precursor protein/Abeta production, and at the same time
17 occurred prior to the appearance of amyloid precursor protein accumulation, an indicator of disrupte
18 embrane alpha-helical portion of the amyloid precursor protein after the latter values were adjusted
21 LTP.SIGNIFICANCE STATEMENT Secreted amyloid precursor protein-alpha (sAPPalpha) is a neurotrophic an
22 ure amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha), analytes central to
23 nce of any changes in the amounts of amyloid precursor protein, amyloid-beta or synaptic proteins.
24 ore, we observed increased levels of amyloid precursor protein and amyloid beta in PITRM1-knockout ne
26 eased phosphorylation of full-length amyloid precursor protein and its associated neurotoxic cleavage
27 tides deriving from the pro-opiomelanocortin precursor protein and localized a specific area of the p
28 ase association with substrates like amyloid precursor protein and N-cadherin, but not with its shedd
31 hods: Nine wild-type (WT) mice and 9 amyloid precursor protein and presenilin 1 double-transgenic (AP
32 s revealed the 3D structure of a macrocyclic precursor protein and provided important mechanistic ins
33 kines of the IL-1 family, are synthesized as precursor proteins and activated by the inflammasome via
34 play important roles in binding amyloid beta precursor proteins and modulating PS1 catalytic activity
35 ides are proteolytically derived from larger precursor proteins and subject to several additional ste
36 pase-3 cleavage site within the amyloid-beta precursor protein, and a caspase-3 cleavage of tau as th
37 GR signaling pathways, processing of amyloid precursor protein, and enzymes involved in Tau phosphory
38 a product of the proteolysis of the amyloid precursor protein APP, is related to Abeta42 by an addit
40 ells bearing the Swedish mutation of amyloid precursor protein (APP(sw) HEK cells) as a cellular mode
41 s disease, as they are produced from amyloid precursor protein (APP) along the endocytic pathway of l
42 ain region-specific up-regulation of amyloid precursor protein (APP) and Abeta (40 and 42) in astrocy
43 teraction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR6) on MN
44 eased Abeta production by modulating amyloid precursor protein (APP) and gamma-secretase levels in li
45 roduct of the ubiquitously expressed amyloid precursor protein (APP) and is able to self-associate in
46 AD, requires the extra gene copy of amyloid precursor protein (APP) and is specifically mediated by
51 rated altered levels of amyloid-beta (Abeta) precursor protein (APP) and its metabolites in FXS and i
52 and gamma-secretase cleavages of the amyloid precursor protein (APP) and mediates a synergistic effec
54 a-, and gamma-secretases, cleave the amyloid precursor protein (APP) and modulate beta-amyloid (Abeta
55 (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 and PSEN2)
56 s) expressing varying levels of amyloid beta precursor protein (APP) and presenilin 1 (PS1) with AD m
57 ExNef caused a redistribution of amyloid precursor protein (APP) and Tau to lipid rafts and incre
58 cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the amyloid-b
59 to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cleaving e
60 turn enhances transcription of amyloid-beta precursor protein (APP) and thereby increases amyloid-be
61 er C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present in cerebrospinal flu
62 and animal models to edit endogenous amyloid precursor protein (APP) at the extreme C-terminus and re
63 biological function of amyloid beta (Abeta) precursor protein (APP) beyond its role in Alzheimer's d
65 a) peptide, derived from cleavage of amyloid precursor protein (APP) by beta- and gamma-secretases.
66 formed by sequential cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE) and gam
67 enerated by a sequential cleavage of amyloid precursor protein (APP) by beta-secretase 1 (BACE-1) fol
69 ived from sequential cleavage of the amyloid precursor protein (APP) by beta-site APP cleaving enzyme
70 otoxic peptide excised from the amyloid-beta precursor protein (APP) by beta-site APP-cleaving enzyme
72 formed by successive cleavage of the amyloid precursor protein (APP) by the beta and gamma secretases
76 imer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by gamma-secretase, inc
79 AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) traffi
80 se, butyrylcholinesterase, beta-site amyloid precursor protein (APP) cleaving enzyme-1 (BACE-1), and
84 ssense mutations in the amyloid beta (Abeta) precursor protein (APP) gene have been implicated in ear
85 dels that one extra copy of a normal amyloid precursor protein (APP) gene impairs lysosomal acidifica
86 as compared to rodent Abeta, the rat Amyloid Precursor Protein (App) gene was mutated to produce huma
89 proteins.SIGNIFICANCE STATEMENT The amyloid precursor protein (App) has been intensively studied for
92 amyloid beta (Abeta) formation from amyloid precursor protein (APP) in vitro To determine whether lo
93 (BACE1) initiates processing of the amyloid precursor protein (APP) into Abeta peptides, which have
94 s responsible for the proteolysis of amyloid precursor protein (APP) into short, aggregation-prone am
95 g body of evidence suggests that the amyloid precursor protein (APP) intracellular C-terminal fragmen
99 ted with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secretase to
100 reveal that the membrane-associated amyloid precursor protein (APP) is highly expressed in macrophag
105 arlier complications occurring while amyloid precursor protein (APP) is trafficking through the early
106 tical slices from male wild-type and amyloid precursor protein (APP) knock-out (KO) mice to assess th
107 ations in Presenilins (PSEN) and the amyloid precursor protein (APP) lead to production of longer amy
109 presenilin (PSH) hypotheses and the amyloid precursor protein (APP) matrix approach (AMA), of which
110 etabolism, tau binding proteins, and amyloid precursor protein (APP) metabolism, showing that genetic
111 retase 1 (BACE-1) and BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted APPbeta, C
112 g human genes such as those encoding amyloid precursor protein (APP) or presenilins (PSEN1 or PSEN2)
114 vement of endosomes and lysosomes in amyloid precursor protein (APP) processing and clearance, and th
115 varepsilon3/4 allele exhibit altered amyloid precursor protein (APP) processing, abnormally increased
118 other mutations at this site of amyloid beta precursor protein (APP) reduced C99 generation and decre
121 eta by the proteolytic processing of amyloid precursor protein (APP) through the endocytic pathway, w
122 ompelling genetic evidence links the amyloid precursor protein (APP) to Alzheimer's disease (AD) and
123 The proteolytic cleavage of beta-amyloid precursor protein (APP) to form the amyloid beta (Abeta)
124 associated with the cleavage of the amyloid precursor protein (APP) to produce the toxic amyloid-bet
125 a pathology and neuroinflammation in amyloid precursor protein (APP) transgenic mice are worsened by
126 ted neurons extracted from preplaque amyloid precursor protein (APP) transgenic rats were found to pr
127 a42) peptide generated from the amyloid-beta precursor protein (APP) via cleavages by beta- and gamma
128 es revealed that the dynamics of the amyloid precursor protein (APP) were significantly impaired.
129 scyllo-inositol, in cells expressing amyloid precursor protein (APP) with the Osaka (E693Delta) mutat
130 thology and astrogliosis in the male amyloid precursor protein (APP)(SWE) /presenilin 1 (PS1)(DeltaE9
132 t of the Alzheimer's disease-related amyloid precursor protein (APP), although neuronal morphology wa
133 Abeta is a cleavage product of the amyloid precursor protein (APP), and aberrant posttranslational
134 erol homeostasis and cleavage of the amyloid precursor protein (APP), and how this relationship relat
135 esulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofibrillary
136 to an interaction between DISC1 and amyloid precursor protein (APP), and to an association of a sing
137 has been considered because the amyloid-beta precursor protein (APP), APP metabolites, and key APP cl
138 icits as well as the upregulation of amyloid precursor protein (APP), BACE-1, a trending increase in
139 hrough sequential proteolysis of the amyloid precursor protein (APP), first by the action of beta-sec
140 otal-Tau, phosphorylated-Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, alphaII-spectrin, a
141 metabolite of sequential cleavage of amyloid precursor protein (APP), is a critical step in the patho
142 linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS).
143 rived from proteolytic processing of amyloid precursor protein (APP), play a central role in AD patho
145 ls overexpress mutant forms of human amyloid precursor protein (APP), producing high levels of amyloi
147 gregates of peptide fragments of the amyloid precursor protein (APP), typically 40 or 42 residues in
148 that of transgenic mice that express amyloid precursor protein (APP), which is duplicated in DS and i
149 ese conditions may be constituted by amyloid precursor protein (APP), which plays a pivotal role in t
150 tein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggregates t
151 rily for its initial cleavage of the amyloid precursor protein (APP), which ultimately leads to the g
153 as recently suggested that beta-site amyloid precursor protein (APP)-cleaving enzyme 2 (BACE2) functi
167 ular amyloidogenic proteins (amylin, amyloid precursor protein [APP], and amyloid-beta [Abeta]) and a
168 sion of the membrane-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1) from the
169 n the Kunitz inhibitor domain of the amyloid precursor protein (APPI) that incorporated a new disulfi
170 e have previously shown that the fly amyloid precursor protein (APPL) is required for memory in the M
171 D) expressing disease-causing mutant amyloid precursor protein (APPsw) and presenilin-1 (PS1DeltaE9)
172 hat mutations in the gene coding for amyloid precursor protein are responsible for autosomal dominant
175 This protein is generated from the composite precursor protein Atp25 upon internal cleavage by the ma
176 Due to the fact that it also cleaves amyloid precursor protein, BACE1 is a therapeutic target in Alzh
177 used a mouse model expressing human amyloid precursor protein bearing two familial mutations and ask
178 roblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the familial doubl
179 d association of variants at amyloid-beta A4 precursor protein-binding family B member 2 (APBB2; chro
180 se (AD) are tied to mutations in the amyloid precursor protein, but the cellular mechanisms that caus
181 s of AD are tied to mutations in the amyloid precursor protein, but the cellular mechanisms that caus
182 is expressed in the form of a large Gag-Pol precursor protein by suppression of translational termin
183 at is generated by thrombin from the zymogen precursor protein C in a reaction greatly accelerated by
184 Intramembrane cleavage of the beta-amyloid precursor protein C99 substrate by gamma-secretase is im
185 om >100 substrates, including Notch, amyloid precursor protein, cadherins, growth factors, and chemok
186 nied by a decrease in BACE1-mediated amyloid precursor protein cleavage and amyloid-beta levels.
187 "endosomal traffic jam" that drives amyloid precursor protein cleavage to amyloid-beta in endosomes.
188 RNA (miR-188-3p) targeting beta-site amyloid precursor protein cleaving enzyme (BACE)-1, a key enzyme
189 nt to unleash a global and beta-site amyloid precursor protein cleaving enzyme 1 (bace-1) DNA demethy
190 Mice were treated with a beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor.
192 gene driven by the BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) promoter, which inc
193 idogenic processing enzyme beta-site amyloid precursor protein cleaving enzyme 1, and both total and
194 Furthermore, increased beta-site amyloid precursor protein-cleaving (APP-cleaving) enzyme 1 (BACE
196 is an orally administered beta-site amyloid precursor protein-cleaving enzyme 1 (BACE-1) inhibitor t
199 ion of an inhibitor of the beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on Alzheimer
201 major target has been the beta-site amyloid-precursor-protein-cleaving enzyme 1 (BACE-1), with many
204 s partially due to overexpression of amyloid precursor protein, encoded by APP, as a result of the lo
207 a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, APLP2), de
208 e released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing
209 ats, such as increased deposition of amyloid precursor protein fragments associated with the appearan
211 Alzheimer's disease (AD)-implicated amyloid precursor protein gene (APP) and comprehensively examine
212 xpress the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupled receptor k
214 neurons and in mice expressing human amyloid precursor protein (hAPP mice), a model for familial AD t
215 the axon of AD-related mutant human amyloid precursor protein (hAPP) transgenic (Tg) mouse neurons.
216 8 (Tg) transgenic mice express human amyloid precursor protein harboring the Swedish and Indiana fami
217 st and human Sde2 are translated as inactive precursor proteins harbouring the ubiquitin-fold domain
219 sm by which such peptides emerge from linear precursor proteins has received increased attention; how
220 ed in anterograde trafficking of the amyloid precursor protein in neurons and in the secretion of tum
221 nduced neurons overexpressing mutant amyloid precursor protein in the background of APOE varepsilon3/
222 mice, which overexpress mutant human amyloid precursor protein in the brain, exhibit two cryptic defi
223 s JNK-interacting protein 1 and amyloid beta precursor protein in the brains and spinal cords of MKK7
225 terative, autocatalytic alpha- N-methylating precursor proteins in the borosin family of ribosomally
227 sAPPbeta (a soluble beta fragment of amyloid precursor protein) in cerebrospinal fluid (CSF) has been
229 ng as synapse-to-nucleus messengers, amyloid precursor protein intracellular domain associated-1 prot
230 and golgi body recycling as well as prolamin precursor proteins involved in refolding of proteins.
231 eature of AD, and endocytosis of the amyloid precursor protein is an important step in its subsequent
232 lzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell types an
234 hippocampal levels of phosphorylated amyloid precursor protein, its pro-amyloidogenic processing enzy
235 "remapping." We tested remapping in amyloid precursor protein knockin (APP-KI) mice with impaired sp
236 primarily due to triplication of the amyloid precursor protein located on chromosome 21, the precise
238 Strikingly, genetic deficiency of the Medin precursor protein, MFG-E8, eliminates not only vascular
242 d with the intracellular accumulation of the precursor protein of Abeta, APP, as a result of the sele
245 ransgenic mice expressing human amyloid-beta precursor protein, presenilin 1, and tau mutations, and
246 intracerebroventricular infusion in amyloid precursor protein/presenilin 1 (APP/PS1) double-transgen
247 of CLU on Abeta pathology using the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of
248 r, and brain tissues in a late-stage amyloid precursor protein/presenilin-1 (APP/PS-1) human transgen
249 s was coupled with reduced levels of amyloid precursor protein processing and Abeta production, compa
250 the latter case, proteins related to amyloid precursor protein processing and secretion are S-nitrosa
251 ransport in regulating amyloidogenic amyloid precursor protein processing and support a model wherein
252 ese swellings contain high levels of amyloid precursor protein processing enzymes (BACE1 and presenil
253 activity without detectably altering amyloid precursor protein processing or extracellular Abeta/beta
254 protein levels and the related amyloid-beta precursor protein processing, amyloid-beta load and eIF4
255 may contribute to amyloidogenic amyloid-beta precursor protein processing, compromise trophic signall
257 levels is not due to a change in mRNA of its precursor protein, proenkephalin, in susceptible mice bu
258 agment of Nogo-A is generated by the amyloid precursor protein protease BACE1 and presented on the me
259 we have uncovered a role for soluble amyloid precursor protein (sAPP) as a vascular niche signal in t
260 -secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, sAPPalpha, glial-derived n
261 ncluding those derived from the same amyloid precursor protein, such as Aeta or sAPPalpha, and autono
262 ransgenic mice expressing human beta-amyloid precursor protein Swedish (Tg-SwDI), a model of cerebrov
263 l signs, astrogliosis, deposition of amyloid precursor protein, synaptic loss and neuronal death were
264 ntified the protein interacting with amyloid precursor protein tail 1 (PAT1) as a potential partner o
267 ansgenic mice overexpressing mutated amyloid precursor protein (Tg2576), Abeta causes dysfunction in
269 The Vgf gene encodes a secretory peptide precursor protein that has critical neuroendocrine funct
271 smembrane proteins, most notably the amyloid precursor protein that results in Abeta, a transmembrane
273 complex involved in the cleavage of amyloid precursor proteins that lead to the formation of amyloid
275 e both contribute to the removal of arrested precursor proteins that specifically accumulate in these
276 -terminal fragment (beta-CTF) from the Abeta precursor protein, the gamma-secretase complex produces
277 proteome from the cytoplasm by translocating precursor proteins through the translocase of the outer
278 s biological importance, the thyroid hormone precursor protein, thyroglobulin (Tg), has been experime
279 Hedgehog (Hh) autoprocessing converts Hh precursor protein to cholesterylated Hh ligand for downs
281 ves the correct folding of the mutant capsid precursor protein to permit virion assembly.IMPORTANCE R
283 s noted in untreated HSCs of postnatal Abeta precursor protein transgenic (APP tg) mice, Abeta deposi
285 RNA data using AD postmortem brains, amyloid precursor protein transgenic mice and AD cell lines.
286 Starting at 5 months of age, tet-off amyloid precursor protein transgenic mice were treated with doxy
288 expectedly, ablation of CR3 in human amyloid precursor protein-transgenic mice results in decreased,
290 TOMM34 and 14-3-3 participated in cytosolic precursor protein transport mediated by the coordinated
292 he cavity of hexon-the cleaved N terminus of precursor protein VI (pVIn), the cleaved N terminus of p
294 eased the import competence of mitochondrial precursor proteins via an extramitochondrial coaggregati
295 protein VI (pVIn), the cleaved N terminus of precursor protein VII (pVIIn2), and mature protein VI.
296 related mutations in presenilin-1 or amyloid precursor protein vs. isogenic gene corrected controls.
297 ed by mutations in the gene encoding amyloid precursor protein, whose processing can result in format
298 ributes to the productive interaction of Tat precursor proteins with the TatBC receptor complex.