ライフサイエンスコーパス: beta-secretase

1 PP distribution in endosomes and cleavage by beta secretase.

2 partyl proteases that has been identified as beta-secretase.

3 ating that meprin beta acts independently of beta-secretase.

4 also process APP in a manner reminiscent of beta-secretase.

5 sterase, self-induced Abeta aggregation, and beta-secretase.

6 g of the substrate's ectodomain by alpha- or beta-secretase.

7 beta-secretase fragment derived from APP by beta-secretase.

8 id precursor protein by either the alpha- or beta-secretase.

9 aving enzyme), has been identified to be the beta-secretase.

10 m of aspartyl proteases and efforts to model beta-secretase.

11 onstrated for enterokinase, caspase-3/7, and beta-secretase.

12 a decrease of the amyloidogenic products of beta-secretase.

13 generated from APP metabolized by alpha- and beta-secretases.

14 s in increased processing by both alpha- and beta-secretases.

15 t of the substrate's ectodomain by alpha- or beta-secretases.

16 he sequential proteolytic cleavage of APP by beta secretase 1 enzyme (BACE1) and gamma-secretase lead

17 Egr-1 silencing also reduces levels of beta-secretase 1 (BACE-1) and BACE-1-cleaved amyloid pre

18 eavage of amyloid precursor protein (APP) by beta-secretase 1 (BACE-1) followed by gamma-secretase.

19 omene was chosen for its radical capture and beta-secretase 1 (BACE-1) inhibitory activities.

20 beta-Secretase 1 (BACE-1) is an attractive therapeutic t

21 in metastasis; MMP-9, in neuropathic pain), beta-secretase 1 (BACE-1, an aspartic protease in Alzhei

22 , in part, explained by a down-regulation of beta-secretase 1 (BACE1) and an up-regulation of ATP-bin

23 beta-secretase 1 (BACE1) is a key enzyme in the generati

24 treatment and siRNA knockdown revealed that beta-secretase 1 (BACE1) is the protease responsible for

25 Genetic deletion of TNFR1 leads to reduced beta-secretase 1 (BACE1) levels and activity.

26 JN down-regulated the levels and activity of beta-secretase 1 (BACE1) protein as well as the expressi

27 Through intravenous delivery of NLC-beta-secretase 1 (BACE1) siRNA complexes we show effecti

28 of beta-C-terminal fragments (CTFs), and of beta-secretase 1 (BACE1) were also reduced, suggesting t

29 validated small molecule inhibitors against beta-secretase 1 (BACE1), the assay was benchmarked with

30 Previous in vitro studies showed that beta-secretase 1 (BACE1), the key-enzyme of amyloidogene

31 e imaging to study a transmembrane protease, beta-secretase 1 (BACE1), whose ectoplasmic and cytoplas

32 ntramembrane proteolysis via the activity of beta-secretase 1 and gamma-secretase, resulting in the g

33 etic inhibitor, 4-fold more selective toward beta-secretase 1 in relation to beta-secretase 2 and 3-f

34 ing depend on clathrin-mediated endocytosis, beta-secretase 1, and interaction with clathrin adaptor

35 ion of 12/15-LO leads to increased levels of beta-secretase-1 (BACE1) mRNA and protein, a significant

36 conserved noncoding antisense transcript for beta-secretase-1 (BACE1), a crucial enzyme in Alzheimer'

37 ctive toward beta-secretase 1 in relation to beta-secretase 2 and 3-fold more resistant to in vitro m

38 tic localization significantly influence its beta secretase activity and amyloid-beta (Abeta) product

39 We also found an increase in beta-secretase activity and a reduction of neprilysin in

40 1 bound exclusively to RAGE, which inhibited beta-secretase activity and Abeta production and suppres

41 pliced transcripts have dramatically reduced beta-secretase activity and promotion of BACE1 alternati

42 We show that increases in BACE and beta-secretase activity are due to posttranslational sta

43 More significantly, elimination of beta-secretase activity blocks the appearance of CCEs, p

44 examined presynaptic cholinergic markers and beta-secretase activity during progressive central nervo

45 to methyl-beta-cyclodextrin, leptin reduces beta-secretase activity in neuronal cells possibly by al

46 74Me and E64d were selected by inhibition of beta-secretase activity in regulated secretory vesicles

47 enetic and biochemical analysis reveals that beta-secretase activity is not required and that high-af

48 BACE1 (beta-secretase activity of the beta-site APP-cleaving en

49 BACE is a transmembrane protease with beta-secretase activity that cleaves the amyloid precurs

50 Abeta generation by (1) directly decreasing beta-secretase activity, (2) reducing expression of all

51 accompanied by a reduction in Abeta42 level, beta-secretase activity, and oxidative damage.

52 nc18a expression induced a small increase in beta-secretase activity, whereas it also intensified the

53 y was increased in the absence of changes in beta-secretase activity.

54 potential therapeutic strategy for lowering beta-secretase activity.

55 ins reduce Abeta levels mostly by regulating beta-secretase activity.

56 pendent mechanism regulating BACE levels and beta-secretase activity.

57 otent in a cell-based assay for reduction of beta-secretase activity.

58 emia in female rats caused a 30% increase in beta-secretase activity.

59 that endoproteolyzed BACE retains measurable beta-secretase activity.

60 F-beta fragments generated by the alpha- and beta-secretases ADAM10 (a disintegrin and metalloprotein

61 beta-Secretase [also known as the beta-site amyloid prec

62 hat inhibit processing of the wild-type (WT) beta-secretase amyloid precursor protein (APP) site, pre

63 Westmark and colleagues have focused on beta-secretase (amyloidogenic) processing and the accumu

64 The interaction of the beta-secretase and alpha-secretase pathway-mediated proc

65 ptides were significantly decreased, as were beta-secretase and beta C-terminal fragment levels, sugg

66 mptive toxic Abeta species that results from beta-secretase and gamma-secretase activity.

67 It reduces both the beta-secretase and gamma-secretase cleavages of the amyl

68 Sequential proteolysis of APP by beta-secretase and gamma-secretase generates Abeta.

69 , which result from the sequential action of beta-secretase and gamma-secretase on amyloid precursor

70 m the Abeta N and C termini are catalyzed by beta-secretase and gamma-secretase, respectively.

71 cursor protein (APP) following processing by beta-secretase and gamma-secretase.

72 CE) exhibits all of the characteristics of a beta-secretase and has been shown to cleave APP at its b

73 BACE-1 has been shown to be the major beta-secretase and is a primary therapeutic target for A

74 al fragments (CTFs) of APP, but the level of beta-secretase and its activity were not affected.

75 Sequential cleavage of APP by beta-secretase and subsequently gamma-secretase generate

76 ursor protein (APP) by the aspartyl protease beta-secretase and the presenilin-dependent protease gam

77 uential proteolytic cleavage of APP first by beta-secretase and then by gamma-secretase.

78 the amyloid precursor protein (APP) and the beta-secretases and gamma-secretases to colocalize in th

79 ge of the amyloid precursor protein (APP) by beta-secretases and gamma-secretases.

80 uding delta- and eta-secretases, alternative beta-secretases) and additional metabolites, some of whi

81 ellular calcium, (2) activation of the BACE1 beta-secretase, and (3) ErbB4 receptor activation.

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.

86 nerated by the combined action of alpha- and beta-secretases, and resident carboxypeptidase.

87 beta in an AD animal model expressing the WT beta-secretase APP site present in the majority of AD pa

88 Thus, expression of both forms of beta-secretase are linked and may play a combined role i

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

91 Whether elevated beta-secretase (BACE) activity is related to plaque form

92 APP can be cleaved by beta-secretase (BACE) and alpha-secretase to produce APP

93 Ser(396) phosphorylation, and decreases both beta-secretase (BACE) and APOEepsilon4 gene expression.

94 ge of the amyloid precursor protein (APP) by beta-secretase (BACE) and gamma-secretase.

95 eable peptidomimetic inhibitors of the human beta-secretase (BACE) are described.

96 peridine templates for use in SAR studies of beta-secretase (BACE) inhibitors and also as versatile l

97 Beta-secretase (BACE) is a critical enzyme in the produc

98 beta-Secretase (BACE) is a prerequisite for amyloidogene

99 Beta-secretase (BACE), a type-I transmembrane aspartyl p

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

102 on triggers the shedding of surface APP in a beta-secretase (BACE)-dependent manner.

103 be rescued by pharmacological modulation of beta-secretase (BACE).

104 e potent, small molecule inhibitors of human beta-secretase (BACE).

105 ine-based peptidomimetic inhibitors of human beta-secretase (BACE).

106 ound beta-amyloid precursor protein (APP) by beta-secretase (BACE).

107 rrent inhibition of the validated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3be

108 series of cyclic amidine-based inhibitors of beta-secretase (BACE-1).

109 carbinamine derived inhibitors of the enzyme beta-secretase (BACE-1).

110 ecific pocket of the aspartic acid protease, beta-secretase (BACE-1).

111 enzymatic partners (the APP cleaving enzymes beta-secretase [BACE] and presenilin-1 [PS-1], and putat

112 e amyloid precursor protein cleaving enzyme (beta-secretase, BACE) in brain.

113 eavage of amyloid precursor protein (APP) by beta-secretase BACE1 initiates the production and accumu

114 Inhibition of beta-secretase BACE1 is considered one of the most promi

115 ng of amyloid precursor protein (APP) by the beta-secretase BACE1 is the initial step of the amyloido

116 The beta-secretase BACE1 is widely known for its pivotal rol

117 d its ability to inhibit the activity of the beta-secretase BACE1, which cleaves the amyloid precurso

118 a concomitant increase in the levels of the beta-secretase BACE1.

119 ceramide post-translationally stabilizes the beta-secretase BACE1.

120 n that bispecific antibodies against TfR and beta-secretase (BACE1 [beta-amyloid cleaving enzyme-1])

121 In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with

122 avages of amyloid precursor protein (APP) by beta-secretase (BACE1) and gamma-secretase.

123 Abeta generation is initiated when beta-secretase (BACE1) cleaves the amyloid precursor pro

124 we found, for the first time, a reduction of beta-secretase (BACE1) enzyme activity, mRNA level and p

125 Lys670 --> Asn and Met671 --> Leu, with the beta-secretase (BACE1) enzyme and their cleavage mechani

126 A growing subset of beta-secretase (BACE1) inhibitors for the treatment of A

127 The beta-secretase (BACE1) initiates processing of the amylo

128 d precursor protein (APP) by the Alzheimer's beta-secretase (BACE1) is a key step in generating amylo

129 Beta-secretase (BACE1) is a type I integral membrane gly

130 In contrast, intracellular trafficking of beta-secretase (BACE1) is not regulated by APP.

131 amyloid (Abeta) peptides and selectivity for beta-secretase (BACE1) over gamma-secretase.

132 of its inhibitory effects on the activity of beta-secretase (BACE1), a key enzyme for generation of b

133 Abeta, as well as the APP processing enzyme, beta-secretase (BACE1), are also increased in CK-p25 mic

134 beta-Secretase (BACE1), the enzyme responsible for the f

135 Of relevance to Alzheimer's disease, beta-secretase (BACE1), the protein that initiates amylo

136 mediated by transcriptional up-regulation of beta-secretase (BACE1), which results in an elevated pro

137 not infected by HPV16, whereas wild-type and beta-secretase (BACE1)-deficient cells were susceptible.

138 ted Abeta peptides appear to be generated by beta-secretase (BACE1)-independent mechanisms and have p

139 important step in its subsequent cleavage by beta-secretase (BACE1).

140 The beta-secretase, BACE1 is a protease needed to generate a

141 tative alpha-secretase, TACE, as well as the beta-secretase, BACE1 were regulated by chronic hypoxia

142 d precursor protein (APP)-cleaving enzyme 1 (beta-secretase, BACE1) initiates amyloidogenic processin

143 Memapsin 2 (beta-secretase, BACE1) is the protease that initiates cl

144 essed along the amyloidogenic pathway by the beta-secretase, BACE1, generating beta-amyloid (Abeta),

145 Because beta-secretase, BACE1, is critical enzyme for Abeta prod

146 antibodies against endosome markers and the beta-secretase, BACE1.

147 Notably, targeting beta-secretase (beta-site amyloid precursor protein (APP

148 Elevated beta-secretase (beta-site amyloid precursor protein-clea

149 e III) is a major physiological substrate of beta-secretase (beta-site amyloid precursor protein-clea

150 dentification of an aspartyl protease as the beta-secretase (beta-site APP cleaving enzyme, BACE) inv

151 tional activity of the promoters of betaAPP, beta-secretase (beta-site APP-cleaving enzyme 1, BACE1),

152 Beta-secretase [beta-site amyloid precursor protein-clea

153 APP, beta-secretase, beta-amyloid, and CTF were significantly

154 lization of amyloid precursor protein (APP), beta-secretase, beta-amyloid, COOH-terminal fragment (CT

155 The beta-secretase, beta-site amyloid precursor protein clea

156 litating the degradation of the APP-cleaving beta-secretase, beta-site APP-cleaving enzyme.

157 APP and beta-secretase, both present on cell surface, are endocy

158 soforms of pancortin can specifically reduce beta-secretase- but not alpha-secretase-mediated cleavag

159 h a loss-of-function mechanism by regulating beta-secretase cleavage of APP and Abeta levels.

160 Prior analysis had suggested that beta-secretase cleavage of APP and binding of an N-termi

161 position in brain results not from increased beta-secretase cleavage of APP but from impaired Abeta/a

162 he transmembrane domain of APP, we find that beta-secretase cleavage of APP is elevated leading to ge

163 These compounds affected beta-secretase cleavage of APP similarly to 1a.

164 1 (BACE1) were also reduced, suggesting that beta-secretase cleavage of APP was reduced in APP/PS1/ta

165 The beta-secretase cleavage of APP, C99, also increased mode

166 We propose that in addition to the reduced beta-secretase cleavage of APP, the impaired propensity

167 expression on Abeta levels is modulated via beta-secretase cleavage of APP.

168 by RNA interference significantly decreased, beta-secretase cleavage of APP.

169 ral extracellular domain of APP and inhibits beta-secretase cleavage of APP.

170 of toxic amyloid-beta peptide, initiated by beta-secretase cleavage of the amyloid precursor protein

171 bent assay measuring only the secreted human beta-secretase cleavage product (APPsbetaswe) of APPswe

172 We found that the enhanced beta-secretase cleavage reduces the anterograde axonal t

173 A detrimental APP mutation at the beta-secretase cleavage site linked to early-onset AD fo

174 We tested the hypothesis that beta-secretase cleavage site mutations of APP alter APP

175 believed to begin at or after the canonical beta-secretase cleavage site within the amyloid beta-pro

176 rate particularly susceptible to alternative beta-secretase cleavage within these microdomains.

177 s were obtained with the direct precursor of beta-secretase cleavage, C99/SPA4CT-FKBP.

178 ollowing APP ectodomain release by alpha- or beta-secretase cleavage.

179 mbrane C-terminal domain of APP liberated by beta-secretase cleavage.

180 tase cleavage and encourages endocytosis and beta-secretase cleavage.

181 myloid precursor protein (APP) and inhibited beta-secretase cleavage.

182 potential drug targets for interfering with beta-secretase cleavage.

183 t not with Swedish mutant APP, which affects beta-secretase cleavage.

184 n to endosomal compartments, involved in APP beta-secretase cleavage.

185 beta also facilitated the oligomerization of beta-secretase cleaved APP C-terminal fragment (C99).

186 ver, unlike BRI2, the binding of BRI3 to the beta-secretase cleaved APP C-terminal fragment is neglig

187 etase inhibitors suggests that the amount of beta-secretase cleaved CTFs (betaCTFs) of APP underlies

188 The beta-secretase-cleaved APP (either beta-C-terminal fragm

189 and APP isoforms and increased secretion of beta-secretase-cleaved APP fragments and amyloid-beta pe

190 d BACE1 elevations and lowered levels of the beta-secretase-cleaved C-terminal fragment of amyloid pr

191 ed in increased levels of secreted Abeta and beta-secretase-cleaved soluble amyloid precursor protein

192 CE1) has been identified as a major neuronal beta-secretase critical for the formation of beta-amyloi

193 Similarly, chemical inhibition of beta-secretase decreased mitochondrial respiration, sugg

194 In addition to amyloid-beta, alpha- or beta-secretase-dependent cleavage of APP also generates

195 and hippocampus-specific accumulation of the beta-secretase-derived betaAPP fragment C99 that is obse

196 e we show that the Abeta rise depends on the beta-secretase-derived C-terminal fragment of APP (betaC

197 Multiple small-molecule inhibitors of the beta-secretase enzyme (BACE1) are under preclinical or c

198 hile, 5XFAD mice exhibited elevations in the beta-secretase enzyme (BACE1) that initiates amyloid-bet

199 The beta-secretase enzyme BACE1 initiates production of the

200 The beta-secretase enzyme BACE1 requires acidic lumen pH for

201 is of amyloid precursor protein (APP) by the beta-secretase enzyme BACE1.

202 ta-site APP cleaving enzyme 1 (BACE1) is the beta-secretase enzyme required for generating pathogenic

203 BACE1 is the beta-secretase enzyme that initiates production of the b

204 The human beta-secretase enzyme, BACE1, mediates a critical step i

205 ta-site APP-cleaving enzyme 1 (BACE1) is the beta-secretase essential for Abeta generation.

206 n also reduce amyloidogenesis by suppressing beta-secretase expression and activities.

207 t experiments seek to examine how modulating beta-secretase expression and activity alters APP proces

208 eavage of amyloid precursor protein (APP) by beta-secretase followed by gamma-secretase cleavage.

209 PP) with consecutive proteolytic processing: beta-secretase, followed by gamma-secretase.

210 aving enzyme 1 (BACE1) is the major neuronal beta-secretase for Abeta generation.

211 aving enzyme 1 (BACE1) is the major neuronal beta-secretase for amyloid-beta generation and is degrad

212 Abeta40 and Abeta42, and reduced C-terminal beta-secretase fragment derived from APP by beta-secreta

213 Identification of the primary beta-secretase gene, BACE1, provides a unique opportunit

214 ocessing of the amyloid precursor protein by beta-secretase generates C99, which subsequently is clea

215 of amyloid precursor protein (APP) first by beta-secretase, generating C99, and then by gamma-secret

216 cursor protein (APP), first by the action of beta-secretase, generating the beta-C-terminal fragment

217 Tg2576 transgenic mice with an inhibitor of beta-secretase, GRL-8234, rescues the age-related cognit

218 Structurally, beta-secretase has a very large binding site (1000 angst

219 A small molecule nonpeptide inhibitor of beta-secretase has been developed, and its binding has b

220 BACE1, the major beta-secretase in neurons is a palmitoylated transmembra

221 Inhibition of BACE1, as the major beta-secretase in vivo with multiple substrates, however

222 ) mice have validated BACE1 as the authentic beta-secretase in vivo.

223 d access to 6-CF(3)-substituted 1,3-thiazine beta-secretase inhibitor 2.

224 d in the absence of BACE1/2 activity using a beta-secretase inhibitor and BACE knock-out cells, indic

225 s a synergistic effect, when combined with a beta-secretase inhibitor, BACE IV.

226 ced cytotoxicity, which can be attenuated by beta-secretase inhibitor.

227 plexes of exceptionally potent and selective beta-secretase inhibitors are described.

228 minohydantoins as potent and selective human beta-secretase inhibitors is reported.

229 minoimidazoles as potent and selective human beta-secretase inhibitors is reported.

230 The inhibition of AbetaPP cleavage by beta-secretase inhibitors significantly suppressed hESC

231 e describe the development of cell-permeable beta-secretase inhibitors that demonstratively inhibit t

232 hesis that the conjugation of peptidomimetic beta-secretase inhibitors with a fragment of amyloid-bet

233 Treatment of purified neurons with beta-secretase inhibitors, but not gamma-secretase inhib

234 line xanthenes as potent and selective human beta-secretase inhibitors.

235 ved an important role in the design of newer beta-secretase inhibitors.

236 d as a surrogate for the design of renin and beta-secretase inhibitors.

237 beta-Secretase initially cleaves APP thereby generating

238 Cleavage of APP by BACE1/beta-secretase initiates the amyloidogenic cascade leadi

239 precursor protein cleaving enzyme 1 (BACE1) (beta-secretase) initiates generation of beta-amyloid (Ab

240 lular trafficking of PS1/gamma-secretase and beta-secretase is less clear.

241 The beta-secretase is membrane-bound aspartyl protease, most

242 Whereas the identity of beta-secretase is no longer in question, the identity of

243 Because beta-secretase is responsible for the amyloidogenic proc

244 Memapsin 2 (BACE, beta-secretase) is a membrane-associated aspartic protea

245 Memapsin 2 (beta-secretase) is a membrane-associated aspartic protea

246 Memapsin 2 (beta-secretase) is the membrane-anchored aspartic protea

247 Memapsin 2 (beta-secretase) is the protease that initiates cleavage

248 BACE, a beta-secretase, is an attractive potential disease-modif

249 ic pathway, redirecting APP to be cleaved by beta-secretase, leading to an additional increase in C99

250 Upon beta-secretase-mediated cleavage of the beta C-terminal

251 of ADAM10 and shifted APP processing toward beta-secretase-mediated cleavage, while enhancing Abeta

252 f alpha-secretase-mediated, in preference to beta-secretase-mediated, cleavage of APP implicates sumo

253 BACE1 (beta-secretase, memapsin 2, Asp2) has emerged as a promi

254 The beta-secretase or beta-site amyloid precursor protein cl

255 beta-secretase (or BACE1) is the key enzyme in the produ

256 The aspartyl protease beta-secretase, or BACE, has been demonstrated to be a k

257 ecursor protein (APP) processing through the beta-secretase pathway and a lowering of CNS amyloid-bet

258 on, which was secondary to a decrease in the beta-secretase pathway.

259 PP internalization, consistent with enhanced beta-secretase processing in the endocytic pathway.

260 ACE-1) is the predominant enzyme involved in beta-secretase processing of APP and is a primary therap

261 These results suggest that the enhanced beta-secretase processing of APP can directly impair the

262 cretase processing (r = -0.86) and decreased beta-secretase processing of beta-amyloid precursor prot

263 Cleavage of APP by beta-secretase produces a 99 amino acid C-terminal fragm

264 nsmembrane region, after prior processing by beta-secretase, producing amyloid beta-peptides Abeta(40

265 In contrast, C99, the beta-secretase product that remains cell associated, cop

266 ional structure of unbound human memapsin 2 (beta-secretase) protease domain determined at 2.0-A reso

267 acutely increases Abeta levels by enhancing beta-secretase protein expression.

268 ged1-Notch1 signaling in KO mice via reduced beta-secretase proteolysis suggests that altered phenoty

269 ed APP provides more substrate for alpha and beta secretase proteolytic cleavages, thereby increasing

270 The Ala-673 residue lies within the beta-secretase recognition sequence and is part of the a

271 otein-cleaving enzyme 1 (BACE1)-the neuronal beta-secretase responsible for producing beta-amyloid (A

272 BACE-1 is the beta-secretase responsible for the initial amyloidogenes

273 Human BACE, also known as beta-secretase, shows promise as a potential therapeutic

274 d by cathepsin B, selectively cleaves the WT beta-secretase site but not the rare Swedish mutant beta

275 Although memapsin 1 hydrolyzes the beta-secretase site of APP, it is not significantly pres

276 meters in mice expressing the Swedish mutant beta-secretase site of APP.

277 f memapsin 2 nor an antibody directed to the beta-secretase site of APPsw had an effect on the uptake

278 hat cleaves amyloid precursor protein at the beta-secretase site to initiate the release of beta-amyl

279 eaves amyloid precursor protein (APP) at the beta-secretase site, giving rise to amyloidogenic peptid

280 atment of London APP mice, expressing the WT beta-secretase site, with these inhibitors resulted in s

281 cretase site but not the rare Swedish mutant beta-secretase site.

282 cleaves the amyloid precursor protein at the beta-secretase site.

283 eaves amyloid precursor protein (APP) at the beta-secretase site.

284 The beta-secretase that executes the first cleavage event is

285 n, is physiologically processed by alpha- or beta-secretases that cleave APP N-terminal to the transm

286 se model of AD pathology, phosphorylation of beta-secretase, the enzyme involved in the formation of

287 beta-Secretase, the rate-limiting enzymatic activity in

288 eptide precursor protein (APP) by gamma- and beta-secretases, the latter known as beta-site APP-cleav

289 -beta in a preventive mode, i.e., gamma- and beta-secretase; the rationale behind these two targets;

290 ely targeted to rafts where it competed with beta-secretase thereby reducing amyloidogenic APP proces

291 that prevents it being cleaved by alpha- or beta-secretase, thereby precluding Abeta generation in t

292 myloid precursor protein (APP) is cleaved by beta-secretase to generate a 99-aa C-terminal fragment (

293 lator SWH that is enzymatically activated by beta-secretase to produce a high affinity copper chelato

294 product may be due to APP shunting from the beta-secretase to the alpha-secretase pathway.

295 of APP by blocking the access of alpha- and beta-secretases to APP.

296 ma-secretase to APP and access of alpha- and beta-secretases to their cleavage APP sequences.

297 A macrocyclic inhibitor of beta-secretase was designed by covalently cross-linking

298 Unlike beta-secretase, which is a monomeric aspartyl protease,

299 closely homologous to memapsin 2 (BACE), or beta-secretase, whose action on beta-amyloid precursor p

300 The beta secretase, widely known as beta-site amyloid precur