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1 ations in presenilin 1, presenilin 2, or the amyloid precursor protein.
2 s alpha-secretase of the Alzheimer's disease amyloid precursor protein.
3 imer disease-associated mutations within the amyloid precursor protein.
4 expressing familial AD-linked forms of human amyloid precursor protein.
5 decreased beta-secretase processing of beta-amyloid precursor protein.
6 toma cells to DDT or DDE increased levels of amyloid precursor protein.
7 ype I membrane proteins, including Notch and amyloid precursor protein.
8 undant in neurons and occurs on both tau and amyloid precursor protein.
9 protein, phosphorylated tau 181, and soluble amyloid precursor protein.
10 carboxyl-terminal fragment (betaCTF) of beta-amyloid precursor protein.
11 secretion by elevating alpha-cleavage of the amyloid precursor protein.
13 d with doxycycline (dox) to suppress further amyloid precursor protein/Abeta production, and at the s
14 hese observations, anterogradely transported amyloid precursor protein accumulated in ligated sciatic
15 ion on transmembrane proteins other than the amyloid precursor protein affects the nervous system is
17 ant factors amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha) and present
18 to measure amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha), analytes ce
19 the absence of any changes in the amounts of amyloid precursor protein, amyloid-beta or synaptic prot
22 C-terminal domain (residues 672-770) of the amyloid precursor protein and is the immediate precursor
23 mice expressing abnormal levels or forms of amyloid precursor protein and its presumed, etiopathogen
24 Using SH-SY5Y cells overexpressing wild-type amyloid precursor protein and pharmacological inhibition
25 Alzheimer's disease we used a double mutant amyloid precursor protein and presenilin 1 (APPswe/PSEN1
26 Here we report that FAD mutations in beta-amyloid precursor protein and presenilin 1 are able to i
27 expression of human familial AD mutations in amyloid precursor protein and presenilin 1 leads to sens
28 nd transgenic APPPS1 mice (overexpression of amyloid precursor protein and presenilin 1 with Swedish
29 r's disease (AD), mice overexpressing mutant amyloid precursor protein and presenilin-1 (APP/PS1) wer
30 numerous proteins besides ApoER2, including amyloid precursor protein and the synaptic adaptor prote
31 at initiates amyloidogenic processing of the amyloid precursor protein and which is a substrate for t
34 at bind a variety of proteins, including the amyloid precursor protein, and that mediate the assembly
35 Abeta43, a product of the proteolysis of the amyloid precursor protein APP, is related to Abeta42 by
37 kidney cells bearing the Swedish mutation of amyloid precursor protein (APP(sw) HEK cells) as a cellu
38 set Alzheimer's disease-causing mutations in amyloid precursor protein (APP(Swe)) and presenilin 1 (P
39 owed significant amounts of beta-amyloid and amyloid precursor protein (APP) aggregates in the cortex
43 eavage product of the ubiquitously expressed amyloid precursor protein (APP) and is able to self-asso
48 ha-, beta-, and gamma-secretases, cleave the amyloid precursor protein (APP) and modulate beta-amyloi
49 uitin aggregates and increased expression of amyloid precursor protein (APP) and phosphorylated tau (
51 ysosomal cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the a
53 beta due to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cl
54 l invasion and colonization by destabilizing amyloid precursor protein (APP) and ZNF395 transcripts,
55 Overexpression and/or abnormal cleavage of amyloid precursor protein (APP) are linked to Alzheimer'
56 es whether C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present in cerebrosp
57 ally neurotoxic Abeta fragments derived from amyloid precursor protein (APP) at synapses may be a key
59 generated during sequential cleavage of the amyloid precursor protein (APP) by beta- and gamma-secre
60 ta (Abeta) peptide, derived from cleavage of amyloid precursor protein (APP) by beta- and gamma-secre
61 and are formed by sequential cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE)
62 eta is generated by a sequential cleavage of amyloid precursor protein (APP) by beta-secretase 1 (BAC
63 ides derived from sequential cleavage of the amyloid precursor protein (APP) by beta-site APP cleavin
64 tion of Abeta peptide from the processing of amyloid precursor protein (APP) by clipping enzymes (bet
65 ovel regulation of proteolytic processing of amyloid precursor protein (APP) by DISC1, a major risk f
70 dels of Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in syn
72 APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling p
73 icits in AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1
78 d beta-peptide (Abeta) species generated via amyloid precursor protein (APP) endoproteolysis and clea
79 reviously that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neuronal iro
82 EG recordings in tet-off mice overexpressing amyloid precursor protein (APP) from birth display frequ
89 ng evidence suggests that the copper-binding amyloid precursor protein (APP) has an essential synapti
90 Activation of nonamyloidogenic processing of amyloid precursor protein (APP) has been hypothesized to
91 p family proteins.SIGNIFICANCE STATEMENT The amyloid precursor protein (App) has been intensively stu
95 ion of amyloid-beta (Abeta) derived from the amyloid precursor protein (APP) in the brain is thought
96 yloid beta (Abeta) peptides originating from amyloid precursor protein (APP) in the endosomal-lysosom
97 ecretase (BACE1) initiates processing of the amyloid precursor protein (APP) into Abeta peptides, whi
98 retase is responsible for the proteolysis of amyloid precursor protein (APP) into short, aggregation-
99 a growing body of evidence suggests that the amyloid precursor protein (APP) intracellular C-terminal
101 transcriptional regulatory complex with the amyloid precursor protein (APP) intracellular domain.
102 retase component, the enzyme responsible for amyloid precursor protein (APP) intramembraneous cleavag
107 associated with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secre
108 Here, we reveal that the membrane-associated amyloid precursor protein (APP) is highly expressed in m
111 nce of earlier complications occurring while amyloid precursor protein (APP) is trafficking through t
112 nked mutations in Presenilins (PSEN) and the amyloid precursor protein (APP) lead to production of lo
114 ACH) and presenilin (PSH) hypotheses and the amyloid precursor protein (APP) matrix approach (AMA), o
118 beta-secretase 1 (BACE-1) and BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted AP
121 death: 50.0 +/- 8.6 years) with mutations in amyloid precursor protein (APP) or presenilin 1 (PSEN1),
124 ly involvement of endosomes and lysosomes in amyloid precursor protein (APP) processing and clearance
125 D) as it results directly in the decrease of amyloid precursor protein (APP) processing through the b
126 of APOE varepsilon3/4 allele exhibit altered amyloid precursor protein (APP) processing, abnormally i
129 and Abeta42 secretion, and the amount of the amyloid precursor protein (APP) secreted at the cell sur
131 mplicated a pathway involving binding of the Amyloid Precursor Protein (APP) to Death Receptor 6 (DR6
132 enic mouse model expressing a mutant form of amyloid precursor protein (APP) to distinguish the impac
133 ns of alpha-syn-containing preparations into amyloid precursor protein (APP) transgenic mice (express
134 hat Abeta pathology and neuroinflammation in amyloid precursor protein (APP) transgenic mice are wors
138 ng studies revealed that the dynamics of the amyloid precursor protein (APP) were significantly impai
139 in, and scyllo-inositol, in cells expressing amyloid precursor protein (APP) with the Osaka (E693Delt
142 in 4 (CNTN4) or one of its binding partners, amyloid precursor protein (APP), a subset of direction-s
144 transport of the Alzheimer's disease-related amyloid precursor protein (APP), although neuronal morph
145 nerated by the proteolytic processing of the amyloid precursor protein (APP), and alterations to this
146 ta levels, alters cell surface expression of amyloid precursor protein (APP), and improves memory in
147 laques resulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofi
148 eferring to an interaction between DISC1 and amyloid precursor protein (APP), and to an association o
150 a-peptide (Abeta), a cleavage product of the amyloid precursor protein (APP), exerts detrimental effe
151 erated through sequential proteolysis of the amyloid precursor protein (APP), first by the action of
152 oid-beta generation from its precursor, beta-amyloid precursor protein (APP), in a competitive manner
153 tide, a metabolite of sequential cleavage of amyloid precursor protein (APP), is a critical step in t
154 ition of amyloid-beta peptides, derived from amyloid precursor protein (APP), is a neuropathological
155 proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (
156 eta), derived from proteolytic processing of amyloid precursor protein (APP), play a central role in
157 and fully penetrant pathogenic mutations in amyloid precursor protein (APP), presenilin 1 and 2 (PSE
160 ) peptide because of increased processing of amyloid precursor protein (APP), resulting in loss of sy
161 Missense mutations in alanine 673 of the amyloid precursor protein (APP), which corresponds to th
162 ilar to that of transgenic mice that express amyloid precursor protein (APP), which is duplicated in
163 tween these conditions may be constituted by amyloid precursor protein (APP), which plays a pivotal r
164 idue protein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggr
169 udies implicate death receptor 6 (DR6) in an amyloid precursor protein (APP)-dependent pathway regula
181 Here, we examined the impact of CXCR3 in the amyloid precursor protein (APP)/presenilin 1 (PS1) trans
182 ne beta-hydroxylase (DBH) knockout mice with amyloid precursor protein (APP)/presenilin-1 (PS1) mice
184 well as an Alzheimer's disease mouse model, amyloid precursor protein (APP)/PSEN1dE9(+/-) (PS1) that
185 Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
186 /Down syndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in
187 (+/-)) in a mouse model of familial AD (FAD; amyloid precursor protein [APP]/presenilin 1 [PS1]) amel
188 he diversion of the membrane-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1)
190 TgF344-AD) expressing disease-causing mutant amyloid precursor protein (APPsw) and presenilin-1 (PS1D
191 criptomic changes in control and mutant beta-amyloid precursor protein (APPSw,Ind) transgenic mice du
192 known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal
193 e result of alterations in expression of the amyloid precursor protein, as confirmed by both immunost
194 transmembrane aspartyl protease that cleaves amyloid precursor protein at the beta-secretase site to
196 SY5Y neuroblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the famili
197 hemistry; white matter showed Abeta and beta-amyloid precursor protein by immunocytochemistry, but no
198 The 99 amino acid C-terminal fragment of amyloid precursor protein (C99), consisting of a single
199 accompanied by a decrease in BACE1-mediated amyloid precursor protein cleavage and amyloid-beta leve
200 recently that autophagy was responsible for amyloid precursor protein cleaved C-terminal fragment (A
201 hway represses the transcription of the beta-amyloid precursor protein cleaving enzyme (BACE1) via bi
202 sufficient to unleash a global and beta-site amyloid precursor protein cleaving enzyme 1 (bace-1) DNA
203 ide derivative, is a high-affinity beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhi
205 nooxazoline xanthene inhibitors of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is d
206 sion causes an increase in APP and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) prot
207 bustly reduces Abeta by inhibiting beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), a k
208 he beta secretase, widely known as beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), ini
209 S6K1 levels reduced translation of beta-site amyloid precursor protein cleaving enzyme 1 and tau, two
211 reduced translation of tau and the beta-site amyloid precursor protein cleaving enzyme 1, a key enzym
214 inistration of an inhibitor of the beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on A
215 gical substrate of beta-secretase (beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1)).
216 One major target has been the beta-site amyloid-precursor-protein-cleaving enzyme 1 (BACE-1), wi
218 of Group II mGluR in Dutch APP (Alzheimer's amyloid precursor protein E693Q) transgenic mice that ac
222 pressing a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, AP
223 s of the Alzheimer's disease (AD)-implicated amyloid precursor protein gene (APP) and comprehensively
225 t over-express the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupled re
226 ocampal neurons and in mice expressing human amyloid precursor protein (hAPP mice), a model for famil
227 compared transgenic mice that express human amyloid precursor protein (hAPP) and patients with mild
228 humans with AD, aging mice expressing human amyloid precursor protein (hAPP) showed increased levels
229 cking in the axon of AD-related mutant human amyloid precursor protein (hAPP) transgenic (Tg) mouse n
230 e mortality and network dysfunction in human amyloid precursor protein (hAPP) transgenic mice, which
233 odel of AD (transgenic mice expressing human amyloid precursor protein [hAPP]) and patients in the ea
234 TgCRND8 (Tg) transgenic mice express human amyloid precursor protein harboring the Swedish and Indi
235 examined [3H]PiB binding and Abeta and beta-amyloid precursor protein immunocytochemistry in autopsy
236 ochemistry for beta-amyloid (Abeta) and beta-amyloid precursor protein in brain tissue were obtained
238 iple similarities, strengthening the role of amyloid precursor protein in normal brain function and d
239 human induced neurons overexpressing mutant amyloid precursor protein in the background of APOE vare
240 l PDAPP mice, which overexpress mutant human amyloid precursor protein in the brain, exhibit two cryp
241 screpancy is likely due to overexpression of amyloid precursor protein in the transformed cellular mo
242 es, enhances the amyloidogenic processing of amyloid precursor protein in these organelles and reduce
244 e of the Alzheimer's disease-associated beta-amyloid precursor protein in vitro and in human embryoni
245 affected brain regions caused by cleavage of amyloid precursor protein into the pathogenic peptide am
249 ogy of Alzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell
250 umulation of the C-terminal fragments of the amyloid precursor protein is inversely correlated with P
252 vine pancreatic trypsin inhibitor (BPTI) and amyloid precursor protein Kunitz protease inhibitor (APP
254 hand, gamma-secretase-mediated processing of amyloid precursor protein leads to the production of amy
256 ) identify novel genetic factors involved in amyloid precursor protein metabolism and (ii) highlight
257 he AD mouse model carrying human mutation of amyloid precursor protein (mhAPP) expressing human Abeta
263 ells via intracerebroventricular infusion in amyloid precursor protein/presenilin 1 (APP/PS1) double-
264 e effect of CLU on Abeta pathology using the amyloid precursor protein/presenilin 1 (APP/PS1) mouse m
265 content of mitochondrial 5-methylcytosine in amyloid precursor protein/presenilin 1 mice along with A
266 t spines and boutons distant from plaques in amyloid precursor protein/presenilin 1-GFP (APPPS1-GFP)
267 al glutathione (mGSH) depletion in older age amyloid precursor protein/presenilin-1 (APP/PS1) mice.
268 endosomes was coupled with reduced levels of amyloid precursor protein processing and Abeta productio
269 In the latter case, proteins related to amyloid precursor protein processing and secretion are S
270 sosome transport in regulating amyloidogenic amyloid precursor protein processing and support a model
272 immunoreactivity without detectably altering amyloid precursor protein processing or extracellular Ab
275 Here, we have uncovered a role for soluble amyloid precursor protein (sAPP) as a vascular niche sig
276 soluble metabolites alpha and beta (soluble amyloid precursor protein (sAPP)alpha, sAPPbeta) and two
277 ), gamma-secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, sAPPalpha, glial-d
278 ht chain (NFL), alpha-synuclein (alpha-syn), amyloid precursor protein soluble metabolites alpha and
279 rsor protein in these organelles and reduces amyloid precursor protein sorting to intraluminal vesicl
280 smic reticulum retrograde transport, affects amyloid precursor protein subcellular localization, cell
281 havioural signs, astrogliosis, deposition of amyloid precursor protein, synaptic loss and neuronal de
284 ral transmembrane proteins, most notably the amyloid precursor protein that results in Abeta, a trans
285 protease complex involved in the cleavage of amyloid precursor proteins that lead to the formation of
286 efflux by lowering tau protein that traffics amyloid precursor protein to facilitate iron efflux.
287 m for Golgi fragmentation and its effects on amyloid precursor protein trafficking and processing in
288 gomeric Abeta or in slices from mutant human amyloid precursor protein transgenic mice (mhAPP J20).
290 dated miRNA data using AD postmortem brains, amyloid precursor protein transgenic mice and AD cell li
292 creases brain beta-amyloid (Abeta) levels in amyloid precursor protein transgenic mice, but no data a
298 of intracellular C-terminal fragments of the amyloid precursor protein via the MVB/lysosomal pathway.
299 e proteolytic fragments of the transmembrane amyloid precursor protein, whereas tau is a brain-specif
300 teins including several, such as tau and the amyloid precursor protein, which are involved in the pat
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