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1 PP distribution in endosomes and cleavage by beta secretase.
2 ating that meprin beta acts independently of beta-secretase.
3 also process APP in a manner reminiscent of beta-secretase.
4 sterase, self-induced Abeta aggregation, and beta-secretase.
5 beta-secretase fragment derived from APP by beta-secretase.
6 id precursor protein by either the alpha- or beta-secretase.
7 aving enzyme), has been identified to be the beta-secretase.
8 m of aspartyl proteases and efforts to model beta-secretase.
9 onstrated for enterokinase, caspase-3/7, and beta-secretase.
10 a decrease of the amyloidogenic products of beta-secretase.
11 utations may control cleavage of beta-APP by beta-secretase.
12 partyl proteases that has been identified as beta-secretase.
13 generated from APP metabolized by alpha- and beta-secretases.
14 t of the substrate's ectodomain by alpha- or beta-secretases.
15 s in increased processing by both alpha- and beta-secretases.
17 eavage of amyloid precursor protein (APP) by beta-secretase 1 (BACE-1) followed by gamma-secretase.
20 , in part, explained by a down-regulation of beta-secretase 1 (BACE1) and an up-regulation of ATP-bin
22 JN down-regulated the levels and activity of beta-secretase 1 (BACE1) protein as well as the expressi
23 of beta-C-terminal fragments (CTFs), and of beta-secretase 1 (BACE1) were also reduced, suggesting t
24 validated small molecule inhibitors against beta-secretase 1 (BACE1), the assay was benchmarked with
25 e imaging to study a transmembrane protease, beta-secretase 1 (BACE1), whose ectoplasmic and cytoplas
26 etic inhibitor, 4-fold more selective toward beta-secretase 1 in relation to beta-secretase 2 and 3-f
27 ing depend on clathrin-mediated endocytosis, beta-secretase 1, and interaction with clathrin adaptor
28 ion of 12/15-LO leads to increased levels of beta-secretase-1 (BACE1) mRNA and protein, a significant
29 conserved noncoding antisense transcript for beta-secretase-1 (BACE1), a crucial enzyme in Alzheimer'
30 ctive toward beta-secretase 1 in relation to beta-secretase 2 and 3-fold more resistant to in vitro m
31 tic localization significantly influence its beta secretase activity and amyloid-beta (Abeta) product
33 1 bound exclusively to RAGE, which inhibited beta-secretase activity and Abeta production and suppres
35 pliced transcripts have dramatically reduced beta-secretase activity and promotion of BACE1 alternati
39 examined presynaptic cholinergic markers and beta-secretase activity during progressive central nervo
41 to methyl-beta-cyclodextrin, leptin reduces beta-secretase activity in neuronal cells possibly by al
42 74Me and E64d were selected by inhibition of beta-secretase activity in regulated secretory vesicles
44 enetic and biochemical analysis reveals that beta-secretase activity is not required and that high-af
46 secretase activity in brain and that loss of beta-secretase activity produces no profound phenotypic
48 Abeta generation by (1) directly decreasing beta-secretase activity, (2) reducing expression of all
50 from BACE knockout mice showed no detectable beta-secretase activity, and primary cortical cultures f
51 nc18a expression induced a small increase in beta-secretase activity, whereas it also intensified the
59 F-beta fragments generated by the alpha- and beta-secretases ADAM10 (a disintegrin and metalloprotein
61 hat inhibit processing of the wild-type (WT) beta-secretase amyloid precursor protein (APP) site, pre
64 ptides were significantly decreased, as were beta-secretase and beta C-terminal fragment levels, sugg
67 , which result from the sequential action of beta-secretase and gamma-secretase on amyloid precursor
70 CE) exhibits all of the characteristics of a beta-secretase and has been shown to cleave APP at its b
73 receptor, mediating the axonal transport of beta-secretase and presenilin-1, and that processing of
76 ursor protein (APP) by the aspartyl protease beta-secretase and the presenilin-dependent protease gam
78 the amyloid precursor protein (APP) and the beta-secretases and gamma-secretases to colocalize in th
80 uding delta- and eta-secretases, alternative beta-secretases) and additional metabolites, some of whi
82 2 (ApoER2) triggers the endocytosis of APP, beta-secretase, and ApoER2 in neuroblastoma cells, leadi
83 show, by using in silico analysis, that APP, beta-secretase, and gamma-secretase subunits contain, in
84 ction, namely, amyloid precursor protein and beta-secretase, and in beta-amyloid metabolism and alter
85 ppear to be a substrate for either alpha- or beta-secretase, and thus bypasses generation of Abeta.
87 beta in an AD animal model expressing the WT beta-secretase APP site present in the majority of AD pa
89 deposition provides functional evidence for beta-secretase as a primary effector in regional amyloid
90 e involved in the generation of Abeta is the beta-secretase BACE, for which powerful inhibitors have
93 Ser(396) phosphorylation, and decreases both beta-secretase (BACE) and APOEepsilon4 gene expression.
96 peridine templates for use in SAR studies of beta-secretase (BACE) inhibitors and also as versatile l
100 ide, we generated 3xTg-AD mice deficient for beta-secretase (BACE), the protease required for Abeta g
101 ll-length recombinant APP as a substrate for beta-secretase (BACE), we have identified a series of co
106 rrent inhibition of the validated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3be
110 enzymatic partners (the APP cleaving enzymes beta-secretase [BACE] and presenilin-1 [PS-1], and putat
114 d its ability to inhibit the activity of the beta-secretase BACE1, which cleaves the amyloid precurso
117 n that bispecific antibodies against TfR and beta-secretase (BACE1 [beta-amyloid cleaving enzyme-1])
121 we found, for the first time, a reduction of beta-secretase (BACE1) enzyme activity, mRNA level and p
122 Lys670 --> Asn and Met671 --> Leu, with the beta-secretase (BACE1) enzyme and their cleavage mechani
125 d precursor protein (APP) by the Alzheimer's beta-secretase (BACE1) is a key step in generating amylo
129 of its inhibitory effects on the activity of beta-secretase (BACE1), a key enzyme for generation of b
130 Abeta, as well as the APP processing enzyme, beta-secretase (BACE1), are also increased in CK-p25 mic
133 mediated by transcriptional up-regulation of beta-secretase (BACE1), which results in an elevated pro
134 not infected by HPV16, whereas wild-type and beta-secretase (BACE1)-deficient cells were susceptible.
135 ted Abeta peptides appear to be generated by beta-secretase (BACE1)-independent mechanisms and have p
137 tative alpha-secretase, TACE, as well as the beta-secretase, BACE1 were regulated by chronic hypoxia
138 d precursor protein (APP)-cleaving enzyme 1 (beta-secretase, BACE1) initiates amyloidogenic processin
143 e III) is a major physiological substrate of beta-secretase (beta-site amyloid precursor protein-clea
145 dentification of an aspartyl protease as the beta-secretase (beta-site APP cleaving enzyme, BACE) inv
146 tional activity of the promoters of betaAPP, beta-secretase (beta-site APP-cleaving enzyme 1, BACE1),
149 lization of amyloid precursor protein (APP), beta-secretase, beta-amyloid, COOH-terminal fragment (CT
153 soforms of pancortin can specifically reduce beta-secretase- but not alpha-secretase-mediated cleavag
156 position in brain results not from increased beta-secretase cleavage of APP but from impaired Abeta/a
157 he transmembrane domain of APP, we find that beta-secretase cleavage of APP is elevated leading to ge
158 1 (BACE1) were also reduced, suggesting that beta-secretase cleavage of APP was reduced in APP/PS1/ta
160 We propose that in addition to the reduced beta-secretase cleavage of APP, the impaired propensity
164 of toxic amyloid-beta peptide, initiated by beta-secretase cleavage of the amyloid precursor protein
165 bent assay measuring only the secreted human beta-secretase cleavage product (APPsbetaswe) of APPswe
169 believed to begin at or after the canonical beta-secretase cleavage site within the amyloid beta-pro
179 beta also facilitated the oligomerization of beta-secretase cleaved APP C-terminal fragment (C99).
180 ver, unlike BRI2, the binding of BRI3 to the beta-secretase cleaved APP C-terminal fragment is neglig
181 etase inhibitors suggests that the amount of beta-secretase cleaved CTFs (betaCTFs) of APP underlies
183 and APP isoforms and increased secretion of beta-secretase-cleaved APP fragments and amyloid-beta pe
184 d BACE1 elevations and lowered levels of the beta-secretase-cleaved C-terminal fragment of amyloid pr
185 ed in increased levels of secreted Abeta and beta-secretase-cleaved soluble amyloid precursor protein
186 CE1) has been identified as a major neuronal beta-secretase critical for the formation of beta-amyloi
189 and hippocampus-specific accumulation of the beta-secretase-derived betaAPP fragment C99 that is obse
190 e we show that the Abeta rise depends on the beta-secretase-derived C-terminal fragment of APP (betaC
191 Multiple small-molecule inhibitors of the beta-secretase enzyme (BACE1) are under preclinical or c
192 hile, 5XFAD mice exhibited elevations in the beta-secretase enzyme (BACE1) that initiates amyloid-bet
197 ta-site APP cleaving enzyme 1 (BACE1) is the beta-secretase enzyme required for generating pathogenic
202 t experiments seek to examine how modulating beta-secretase expression and activity alters APP proces
203 eavage of amyloid precursor protein (APP) by beta-secretase followed by gamma-secretase cleavage.
206 aving enzyme 1 (BACE1) is the major neuronal beta-secretase for amyloid-beta generation and is degrad
208 Abeta40 and Abeta42, and reduced C-terminal beta-secretase fragment derived from APP by beta-secreta
210 ocessing of the amyloid precursor protein by beta-secretase generates C99, which subsequently is clea
211 of amyloid precursor protein (APP) first by beta-secretase, generating C99, and then by gamma-secret
212 cursor protein (APP), first by the action of beta-secretase, generating the beta-C-terminal fragment
213 Tg2576 transgenic mice with an inhibitor of beta-secretase, GRL-8234, rescues the age-related cognit
214 A small molecule nonpeptide inhibitor of beta-secretase has been developed, and its binding has b
215 t was not known whether BACE was the primary beta-secretase in mammalian brain nor whether inhibition
219 d in the absence of BACE1/2 activity using a beta-secretase inhibitor and BACE knock-out cells, indic
225 e describe the development of cell-permeable beta-secretase inhibitors that demonstratively inhibit t
226 hesis that the conjugation of peptidomimetic beta-secretase inhibitors with a fragment of amyloid-bet
232 precursor protein cleaving enzyme 1 (BACE1) (beta-secretase) initiates generation of beta-amyloid (Ab
244 ic pathway, redirecting APP to be cleaved by beta-secretase, leading to an additional increase in C99
245 of ADAM10 and shifted APP processing toward beta-secretase-mediated cleavage, while enhancing Abeta
246 f alpha-secretase-mediated, in preference to beta-secretase-mediated, cleavage of APP implicates sumo
248 in mammalian brain nor whether inhibition of beta-secretase might have effects in mammals that would
252 ecursor protein (APP) processing through the beta-secretase pathway and a lowering of CNS amyloid-bet
254 PP internalization, consistent with enhanced beta-secretase processing in the endocytic pathway.
255 ACE-1) is the predominant enzyme involved in beta-secretase processing of APP and is a primary therap
256 These results suggest that the enhanced beta-secretase processing of APP can directly impair the
257 cretase processing (r = -0.86) and decreased beta-secretase processing of beta-amyloid precursor prot
259 nsmembrane region, after prior processing by beta-secretase, producing amyloid beta-peptides Abeta(40
261 ional structure of unbound human memapsin 2 (beta-secretase) protease domain determined at 2.0-A reso
263 ged1-Notch1 signaling in KO mice via reduced beta-secretase proteolysis suggests that altered phenoty
264 ed APP provides more substrate for alpha and beta secretase proteolytic cleavages, thereby increasing
266 otein-cleaving enzyme 1 (BACE1)-the neuronal beta-secretase responsible for producing beta-amyloid (A
269 , in cells BACE2 has a limited effect on the beta-secretase site but efficiently cleaves the sequence
270 d by cathepsin B, selectively cleaves the WT beta-secretase site but not the rare Swedish mutant beta
273 f memapsin 2 nor an antibody directed to the beta-secretase site of APPsw had an effect on the uptake
274 tically active and specific for cleaving the beta-secretase site of human APP, as demonstrated with s
275 hat cleaves amyloid precursor protein at the beta-secretase site to initiate the release of beta-amyl
276 oid precursor protein (APP) sequences at the beta-secretase site, and near the alpha-secretase site,
277 eaves amyloid precursor protein (APP) at the beta-secretase site, giving rise to amyloidogenic peptid
278 atment of London APP mice, expressing the WT beta-secretase site, with these inhibitors resulted in s
283 n, is physiologically processed by alpha- or beta-secretases that cleave APP N-terminal to the transm
284 se model of AD pathology, phosphorylation of beta-secretase, the enzyme involved in the formation of
286 eptide precursor protein (APP) by gamma- and beta-secretases, the latter known as beta-site APP-cleav
287 -beta in a preventive mode, i.e., gamma- and beta-secretase; the rationale behind these two targets;
288 ely targeted to rafts where it competed with beta-secretase thereby reducing amyloidogenic APP proces
289 that prevents it being cleaved by alpha- or beta-secretase, thereby precluding Abeta generation in t
290 myloid precursor protein (APP) is cleaved by beta-secretase to generate a 99-aa C-terminal fragment (
291 lator SWH that is enzymatically activated by beta-secretase to produce a high affinity copper chelato
297 BACE1 has been identified as the Alzheimer's beta-secretase, whereas BACE2 was mapped to the Down's c
300 closely homologous to memapsin 2 (BACE), or beta-secretase, whose action on beta-amyloid precursor p
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