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1 n presenilin 1, presenilin 2, or the amyloid precursor protein.
2 secretase of the Alzheimer's disease amyloid precursor protein.
3 esterol for the correct processing of the Hh precursor protein.
4 Hh ligand, generated by autoprocessing of Hh precursor protein.
5 ease-associated mutations within the amyloid precursor protein.
6 ng familial AD-linked forms of human amyloid precursor protein.
7 4 following proteolytic cleavage of pro-NRG1 precursor protein.
8 ed beta-secretase processing of beta-amyloid precursor protein.
9 phosphorylated tau 181, and soluble amyloid precursor protein.
10 bial peptides are derived from nonfunctional precursor proteins.
11 ion involves proteolytic processing of seven precursor proteins.
12 cleaving transport signals off translocated precursor proteins.
13 of plant life and are usually synthesized as precursor proteins.
14 were connected to APP (encoding amyloid beta precursor protein), a major player in Alzheimer's diseas
16 oxycycline (dox) to suppress further amyloid precursor protein/Abeta production, and at the same time
17 sits in Alzheimer disease brain and in Abeta precursor protein (AbetaPP) transgenic mouse models.
18 ervations, anterogradely transported amyloid precursor protein accumulated in ligated sciatic nerves
19 ransmembrane proteins other than the amyloid precursor protein affects the nervous system is only beg
20 Sarm1(-/-) mice developed fewer beta-amyloid precursor protein aggregates in axons of the corpus call
21 ors amyloid beta (Abeta) and soluble amyloid precursor protein-alpha (sAPPalpha) and present novel fi
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.
25 tides deriving from the pro-opiomelanocortin precursor protein and localized a specific area of the p
26 er's disease we used a double mutant amyloid precursor protein and presenilin 1 (APPswe/PSEN1dE9) mou
27 on of human familial AD mutations in amyloid precursor protein and presenilin 1 leads to sensitivity
29 s revealed the 3D structure of a macrocyclic precursor protein and provided important mechanistic ins
30 xcision of the internal intein domain from a precursor protein and the concomitant ligation of the fl
31 ates amyloidogenic processing of the amyloid precursor protein and which is a substrate for these pro
32 kines of the IL-1 family, are synthesized as precursor proteins and activated by the inflammasome via
33 play important roles in binding amyloid beta precursor proteins and modulating PS1 catalytic activity
34 pase-3 cleavage site within the amyloid-beta precursor protein, and a caspase-3 cleavage of tau as th
37 a variety of proteins, including the amyloid precursor protein, and that mediate the assembly of mult
38 are derived from 1 of several amyloidogenic precursor proteins, and the prognosis of the disease is
39 a product of the proteolysis of the amyloid precursor protein APP, is related to Abeta42 by an addit
41 ells bearing the Swedish mutation of amyloid precursor protein (APP(sw) HEK cells) as a cellular mode
42 eimer's disease-causing mutations in amyloid precursor protein (APP(Swe)) and presenilin 1 (PSEN1(M14
43 vious studies have demonstrated that amyloid precursor protein (APP) and Abeta levels can be increase
44 SorLA interacts directly with the amyloid precursor protein (APP) and affects the processing of th
45 roduct of the ubiquitously expressed amyloid precursor protein (APP) and is able to self-associate in
50 rated altered levels of amyloid-beta (Abeta) precursor protein (APP) and its metabolites in FXS and i
52 a-, and gamma-secretases, cleave the amyloid precursor protein (APP) and modulate beta-amyloid (Abeta
53 cysteine protease that cleaves both amyloid precursor protein (APP) and tau, mediating the amyloid-b
55 to a change in the approximation of amyloid precursor protein (APP) and the beta-site APP cleaving e
56 turn enhances transcription of amyloid-beta precursor protein (APP) and thereby increases amyloid-be
57 er C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present in cerebrospinal flu
58 rotoxic Abeta fragments derived from amyloid precursor protein (APP) at synapses may be a key contrib
60 a) peptide, derived from cleavage of amyloid precursor protein (APP) by beta- and gamma-secretases.
61 formed by sequential cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE) and gam
62 enerated by a sequential cleavage of amyloid precursor protein (APP) by beta-secretase 1 (BACE-1) fol
63 ived from sequential cleavage of the amyloid precursor protein (APP) by beta-site APP cleaving enzyme
64 Abeta peptide from the processing of amyloid precursor protein (APP) by clipping enzymes (beta- and g
65 ulation of proteolytic processing of amyloid precursor protein (APP) by DISC1, a major risk factor fo
70 Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in synaptic pl
72 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling pathways
75 AD.SIGNIFICANCE STATEMENT beta-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) traffi
78 y that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neuronal iron export
84 ssense mutations in the amyloid beta (Abeta) precursor protein (APP) gene have been implicated in ear
88 proteins.SIGNIFICANCE STATEMENT The amyloid precursor protein (App) has been intensively studied for
92 ta (Abeta) peptides originating from amyloid precursor protein (APP) in the endosomal-lysosomal compa
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
100 ted with Alzheimer disease (AD), the amyloid precursor protein (APP) is cleaved by beta-secretase to
101 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 ations in Presenilins (PSEN) and the amyloid precursor protein (APP) lead to production of longer amy
108 presenilin (PSH) hypotheses and the amyloid precursor protein (APP) matrix approach (AMA), of which
112 retase 1 (BACE-1) and BACE-1-cleaved amyloid precursor protein (APP) metabolites (secreted APPbeta, C
115 vement of endosomes and lysosomes in amyloid precursor protein (APP) processing and clearance, and th
116 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
119 a42 secretion, and the amount of the amyloid precursor protein (APP) secreted at the cell surface was
120 ompelling genetic evidence links the amyloid precursor protein (APP) to Alzheimer's disease (AD) and
121 pha-syn-containing preparations into amyloid precursor protein (APP) transgenic mice (expressing APP6
122 a pathology and neuroinflammation in amyloid precursor protein (APP) transgenic mice are worsened by
123 Here, we report that cAMP controls amyloid precursor protein (APP) translation and Abeta levels, an
125 es revealed that the dynamics of the amyloid precursor protein (APP) were significantly impaired.
126 scyllo-inositol, in cells expressing amyloid precursor protein (APP) with the Osaka (E693Delta) mutat
128 ouse leads to downregulation of amyloid-beta precursor protein (APP), a known neuronal migration gene
130 TN4) or one of its binding partners, amyloid precursor protein (APP), a subset of direction-selective
131 t of the Alzheimer's disease-related amyloid precursor protein (APP), although neuronal morphology wa
132 esulting from abnormal processing of amyloid precursor protein (APP), and presence of neurofibrillary
133 to an interaction between DISC1 and amyloid precursor protein (APP), and to an association of a sing
134 hrough sequential proteolysis of the amyloid precursor protein (APP), first by the action of beta-sec
136 metabolite of sequential cleavage of amyloid precursor protein (APP), is a critical step in the patho
137 amyloid-beta peptides, derived from amyloid precursor protein (APP), is a neuropathological hallmark
138 linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS).
139 rived from proteolytic processing of amyloid precursor protein (APP), play a central role in AD patho
141 ndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in both DS
142 ndrome critical region 1 (DSCR1) and amyloid-precursor protein (APP), proteins upregulated in both DS
144 e because of increased processing of amyloid precursor protein (APP), resulting in loss of synapses a
145 that of transgenic mice that express amyloid precursor protein (APP), which is duplicated in DS and i
146 ese conditions may be constituted by amyloid precursor protein (APP), which plays a pivotal role in t
147 tein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggregates t
151 plicate death receptor 6 (DR6) in an amyloid precursor protein (APP)-dependent pathway regulating dev
159 examined the impact of CXCR3 in the amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mo
161 ins of Alzheimer's patients and amyloid-beta precursor protein (APP)/PS1 transgenic mice were signifi
162 an Alzheimer's disease mouse model, amyloid precursor protein (APP)/PSEN1dE9(+/-) (PS1) that lacked
163 sion of the membrane-bound beta-site amyloid precursor protein-(APP) cleaving enzyme (BACE1) from the
164 e have previously shown that the fly amyloid precursor protein (APPL) is required for memory in the M
165 D) expressing disease-causing mutant amyloid precursor protein (APPsw) and presenilin-1 (PS1DeltaE9)
166 hat mutations in the gene coding for amyloid precursor protein are responsible for autosomal dominant
168 f functional ASRGL1 and leaving the inactive precursor protein as a destabilized and aggregation-pron
169 of alterations in expression of the amyloid precursor protein, as confirmed by both immunostaining a
170 This protein is generated from the composite precursor protein Atp25 upon internal cleavage by the ma
171 Due to the fact that it also cleaves amyloid precursor protein, BACE1 is a therapeutic target in Alzh
172 roblastoma cells expressing the beta-amyloid precursor protein (betaAPP) harboring the familial doubl
173 is expressed in the form of a large Gag-Pol precursor protein by suppression of translational termin
174 nied by a decrease in BACE1-mediated amyloid precursor protein cleavage and amyloid-beta levels.
175 resses the transcription of the beta-amyloid precursor protein cleaving enzyme (BACE1) via binding of
176 nt to unleash a global and beta-site amyloid precursor protein cleaving enzyme 1 (bace-1) DNA demethy
177 vative, is a high-affinity beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitor cu
179 ses an increase in APP and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) protein, but
180 els reduced translation of beta-site amyloid precursor protein cleaving enzyme 1 and tau, two key pro
182 translation of tau and the beta-site amyloid precursor protein cleaving enzyme 1, a key enzyme in the
185 ion of an inhibitor of the beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) on Alzheimer
187 major target has been the beta-site amyloid-precursor-protein-cleaving enzyme 1 (BACE-1), with many
189 therapeutic agents that bind specifically to precursor protein conformations and inhibit amyloid asse
193 p II mGluR in Dutch APP (Alzheimer's amyloid precursor protein E693Q) transgenic mice that accumulate
197 a shorter FE65 isoform able to bind amyloid precursor protein family members (APP, APLP1, APLP2), de
198 ense mutations in prodynorphin, encoding the precursor protein for the opioid neuropeptides alpha-neo
199 Alzheimer's disease (AD)-implicated amyloid precursor protein gene (APP) and comprehensively examine
200 Recently, a rare variant in the amyloid precursor protein gene (APP) was described in a populati
202 xpress the Swedish mutant human beta-amyloid precursor protein gene with G protein-coupled receptor k
204 RNA polymerase protein (RdRp), glycoprotein precursor protein, glycoproteins Gn and Gc, as well as p
205 neurons and in mice expressing human amyloid precursor protein (hAPP mice), a model for familial AD t
206 d transgenic mice that express human amyloid precursor protein (hAPP) and patients with mild cognitiv
207 with AD, aging mice expressing human amyloid precursor protein (hAPP) showed increased levels of astr
208 the axon of AD-related mutant human amyloid precursor protein (hAPP) transgenic (Tg) mouse neurons.
209 ity and network dysfunction in human amyloid precursor protein (hAPP) transgenic mice, which simulate
212 AD (transgenic mice expressing human amyloid precursor protein [hAPP]) and patients in the earlier mi
213 8 (Tg) transgenic mice express human amyloid precursor protein harboring the Swedish and Indiana fami
214 st and human Sde2 are translated as inactive precursor proteins harbouring the ubiquitin-fold domain
216 sm by which such peptides emerge from linear precursor proteins has received increased attention; how
217 s how FGLK motifs are required for efficient precursor protein import and how these elements may perm
218 in ovalbumin (OVA) were found to release the precursor protein in a slow and steady manner over an ex
220 ilarities, strengthening the role of amyloid precursor protein in normal brain function and developme
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
226 Alzheimer's disease-associated beta-amyloid precursor protein in vitro and in human embryonic kidney
228 Purification-tagged Toc159 in the absence of precursor protein, indicating spontaneous and translocat
229 brain regions caused by cleavage of amyloid precursor protein into the pathogenic peptide amyloid-be
231 translocases drive the import of beta-barrel precursor proteins into the mitochondrial outer membrane
234 lzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell types an
236 creatic trypsin inhibitor (BPTI) and amyloid precursor protein Kunitz protease inhibitor (APPI), and
237 overexpressing amyloid beta-peptide (Abeta) precursor protein leads to early cerebral microvascular
245 d with the intracellular accumulation of the precursor protein of Abeta, APP, as a result of the sele
247 pending upon the intrinsic properties of the precursor protein/peptide and experimental conditions su
250 ransgenic mice expressing human amyloid-beta precursor protein, presenilin 1, and tau mutations, and
251 intracerebroventricular infusion in amyloid precursor protein/presenilin 1 (APP/PS1) double-transgen
252 of CLU on Abeta pathology using the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of
253 of mitochondrial 5-methylcytosine in amyloid precursor protein/presenilin 1 mice along with Alzheimer
254 and boutons distant from plaques in amyloid precursor protein/presenilin 1-GFP (APPPS1-GFP) nor thos
256 hesized in the endoplasmic reticulum, the CD-precursor protein (pro-CD) is transported through endoso
257 s was coupled with reduced levels of amyloid precursor protein processing and Abeta production, compa
258 the latter case, proteins related to amyloid precursor protein processing and secretion are S-nitrosa
259 ransport in regulating amyloidogenic amyloid precursor protein processing and support a model wherein
260 ese swellings contain high levels of amyloid precursor protein processing enzymes (BACE1 and presenil
261 activity without detectably altering amyloid precursor protein processing or extracellular Abeta/beta
264 ted the expression of Il18 mRNA and inactive precursor protein (proIL-18) in intestinal epithelial ce
266 cleavage of the inactive SREBP transmembrane precursor protein, RIP of the anchor intermediate by sit
267 we have uncovered a role for soluble amyloid precursor protein (sAPP) as a vascular niche signal in t
268 metabolites alpha and beta (soluble amyloid precursor protein (sAPP)alpha, sAPPbeta) and two neuroin
269 -secretase, soluble Abeta42, soluble amyloid precursor protein (sAPP)beta, sAPPalpha, glial-derived n
270 (NFL), alpha-synuclein (alpha-syn), amyloid precursor protein soluble metabolites alpha and beta (so
271 iculum retrograde transport, affects amyloid precursor protein subcellular localization, cell-surface
272 l signs, astrogliosis, deposition of amyloid precursor protein, synaptic loss and neuronal death were
276 smembrane proteins, most notably the amyloid precursor protein that results in Abeta, a transmembrane
277 mal genes that encode cytosolic proteins and precursor proteins that are synthesized in the cytosol f
279 complex involved in the cleavage of amyloid precursor proteins that lead to the formation of amyloid
280 s biological importance, the thyroid hormone precursor protein, thyroglobulin (Tg), has been experime
283 s noted in untreated HSCs of postnatal Abeta precursor protein transgenic (APP tg) mice, Abeta deposi
286 RNA data using AD postmortem brains, amyloid precursor protein transgenic mice and AD cell lines.
287 Starting at 5 months of age, tet-off amyloid precursor protein transgenic mice were treated with doxy
288 brain beta-amyloid (Abeta) levels in amyloid precursor protein transgenic mice, but no data are avail
290 expectedly, ablation of CR3 in human amyloid precursor protein-transgenic mice results in decreased,
292 eta rapidly, with no reactivity to the Abeta precursor protein, transthyretin amyloid aggregates, or
293 he cavity of hexon-the cleaved N terminus of precursor protein VI (pVIn), the cleaved N terminus of p
294 rives from a C-terminal fragment of a larger precursor protein via a caspase-3 mediated cleavage.
296 eased the import competence of mitochondrial precursor proteins via an extramitochondrial coaggregati
297 protein VI (pVIn), the cleaved N terminus of precursor protein VII (pVIIn2), and mature protein VI.
298 resequence translocase (TIM23 complex) sorts precursor proteins with a cleavable presequence either i
299 ributes to the productive interaction of Tat precursor proteins with the TatBC receptor complex.
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