ライフサイエンスコーパス: gamma-secretase inhibitor

1 odies, RNA interference, receptor decoys and gamma-secretase inhibitors).

2 leukemic mice treated with vehicle or with a gamma-secretase inhibitor.

3 ocked in newborn mice by administration of a gamma-secretase inhibitor.

4 e lungs by disrupting Notch signaling with a gamma-secretase inhibitor.

5 nd-dependent Notch signaling is blocked by a gamma-secretase inhibitor.

6 ing of this radioligand or a non-radioactive gamma-secretase inhibitor.

7 (1) arrest and apoptosis when treated with a gamma-secretase inhibitor.

8 eoisomer of LY-411,575, which is a very weak gamma-secretase inhibitor.

9 to a biotinylated, benzophenone-derivatized gamma-secretase inhibitor.

10 ity probe based on a transition state analog gamma-secretase inhibitor.

11 n induction of apoptosis, in the presence of gamma-secretase inhibitor.

12 ofiles observed in humans upon dosing with a gamma-secretase inhibitor.

13 minutes of blocking Abeta production with a gamma-secretase inhibitor.

14 ich is abrogated by combination therapy with gamma secretase inhibitors.

15 inhibitors of PI3K kinase but insensitive to gamma-secretase inhibitors.

16 rminal fragment in mediating the activity of gamma-secretase inhibitors.

17 chema, we avoided the reported toxicities of gamma-secretase inhibitors.

18 was blocked by ATP itself and APP-selective gamma-secretase inhibitors.

19 s, as well as wild-type neurons treated with gamma-secretase inhibitors.

20 eavages, in the presence or absence of known gamma-secretase inhibitors.

21 ial target of a number of recently developed gamma-secretase inhibitors.

22 by inhibitors known as non-transition state gamma-secretase inhibitors.

23 dies of SPP as well as evaluation of SPP and gamma-secretase inhibitors.

24 This function of PS1 is unaffected by gamma-secretase inhibitors.

25 This process can be blocked by gamma-secretase inhibitors.

26 ble that Notch function could be affected by gamma-secretase inhibitors.

27 dominant-negative form of PS or treated with gamma-secretase inhibitors.

28 the active chair conformation of the parent gamma-secretase inhibitors.

29 substrates for assessing relative potency of gamma-secretase inhibitors.

30 showed reduced sensitivity to inhibition by gamma-secretase inhibitors.

31 with NOTCH1-binding sites are insensitive to gamma-secretase inhibitors.

32 get genes, and exhibited cross-resistance to gamma-secretase inhibitors.

33 signaling that can be effectively blocked by gamma-secretase inhibitors.

34 ed by Notch1 signaling and can be blocked by gamma-secretase inhibitors.

35 l, para-substituted fluorophenyl ring in the gamma-secretase inhibitor 1 (BMS-708,163) with the bicyc

36 gulated upon treatment with the Ac-gamma-Glu-gamma-secretase-inhibitor 13a.

37 ric synthesis of novel, potent photoreactive gamma-secretase inhibitors 2 and 3 has been accomplished

38 In contrast to gamma-secretase inhibitors, Abeta42-lowering NSAIDs do n

39 dent protein kinase (PKG) inhibitor, but not gamma-secretase inhibitor, abolished the elevation of sy

40 logic inhibition of Notch activation using a gamma-secretase inhibitor ameliorated TIF.

41 Targeting Notch pathway with gamma-secretase inhibitor and a decoy protein in the for

42 Using gamma-secretase inhibitor and erlotinib in a xenograft m

43 We tested the efficacy of gamma-secretase inhibitor and gamma-secretase modulator

44 lular proliferation, which was suppressed by gamma-secretase inhibitor and Notch3 siRNA.

45 Inactivation of Notch3 by both gamma-secretase inhibitor and Notch3-specific small inte

46 efore relevant factors in the development of gamma-secretase inhibitors and can be evaluated using ap

47 ion by anti-amyloidogenic compounds, such as gamma-secretase inhibitors and nonsteroidal anti-inflamm

48 ME NOTCH1 mutants are effectively blocked by gamma-secretase inhibitors and require an intact metallo

49 duction of DCC-ICD is inhibited by selective gamma-secretase inhibitors, and by the expression of the

50 aceable by peptidomimetic and small molecule gamma-secretase inhibitors, and exhibited rapid associat

51 deficient for gamma-secretase or exposed to gamma-secretase inhibitors are caused by the loss of Not

52 Notch inhibitory agents, such as gamma-secretase inhibitors, are being investigated as ca

53 anti-angiogenesis agent bevacizumab or to a gamma-secretase inhibitor as well as knockdown shRNA stu

54 is on the promise and challenges in applying gamma-secretase inhibitors as a new line of targeted the

55 g is the main cause for untoward effects for gamma-secretase inhibitors as therapeutics for Alzheimer

56 d selective targeting, we have developed the gamma-secretase inhibitor-based prodrugs 13a and 15a as

57 ation of Notch-1 by small interfering RNA or gamma-secretase inhibitors before TW-37 treatment result

58 se embryos revealed 50 and 80% reductions of gamma-secretase inhibitor binding density in the heteroz

59 r radioligands were used to evaluate SPP and gamma-secretase inhibitor binding pharmacology.

60 nhibitory protein (c-FLIP) turnover and that gamma-secretase inhibitor blocked c-FLIP turnover and al

61 he inhibition of IL-5, because addition of a gamma-secretase inhibitor blocked the type I IFN-indepen

62 ependent on secretase activity as ADAM10 and gamma-secretase inhibitors blocked RAGE ligand-mediated

63 observed in rat brain after dosing with the gamma-secretase inhibitor BMS-299897.

64 Instead, membrane-permeable gamma-secretase inhibitors, but not a membrane-impermeab

65 plore the mechanisms of structurally diverse gamma-secretase inhibitors by examining their ability to

66 e specificity or the preference of the known gamma-secretase inhibitors by examining their effects on

67 sion and (ii) selectivity of various SPP and gamma-secretase inhibitors can be rapidly evaluated.

68 Here, we report that gamma-secretase inhibitors can block all Notch signals i

69 Third, gamma-secretase inhibitors can enhance the production of

70 Unexpectedly gamma-secretase inhibitors can increase the secretion of

71 rons with beta-secretase inhibitors, but not gamma-secretase inhibitors, caused significant reduction

72 When the cells were incubated with gamma-secretase inhibitor Compound E, it caused a 2-fold

73 tants and wild-type embryos treated with the gamma-secretase inhibitor, Compound E.

74 gamma-Secretase inhibitors confirmed that enzymatic acti

75 The growth-inhibitory effect of gamma-secretase inhibitor could be partially reversed by

76 nd altered processing of these substrates by gamma-secretase inhibitors could lead to unintended biol

77 or systemic injection of Jagged1 peptide and gamma secretase inhibitor DAPT, respectively.

78 Inhibition of Notch signaling using gamma secretase inhibitors DAPT and L-685,458 or anti-Ja

79 is dependent on Notch signaling, because the gamma-secretase inhibitor DAPT blocked its upregulation.

80 rsely, IL-33 expression was inhibited by the gamma-secretase inhibitor DAPT or by inhibiting the func

81 Abrogation of Notch signaling with the gamma-secretase inhibitor DAPT revealed that Notch and m

82 Using gamma-secretase inhibitor DAPT to acutely block canonica

83 lidate a protocol that utilizes BMP4 and the gamma-secretase inhibitor DAPT to induce SE differentiat

84 tch activation in the chick embryo using the gamma-secretase inhibitor DAPT, we see a complete loss o

85 promote neuronal differentiation such as the gamma-secretase inhibitor DAPT.

86 e metalloproteinase inhibitor GM6001 and the gamma-secretase inhibitor DAPT.

87 blockade of Notch signaling pathways using a gamma-secretase inhibitor, DAPT (N-[N-(3,5-difluorophena

88 Treatment of explants with a gamma-secretase inhibitor, DAPT, decreased Fgf20 mRNA, s

89 d cell death, whereas Notch1 inhibition by a gamma-secretase inhibitor, DAPT, enhanced cell death in

90 otch receptor cleavage was blocked using the gamma-secretase inhibitor, DAPT, or signaling was activa

91 Treatment with the gamma-secretase inhibitor, DAPT, to inhibit cleavage and

92 Exposure of cells to the gamma-secretase inhibitor-DAPT or silencing of Notch1 re

93 Metalloproteinase or gamma-secretase inhibitors decrease adenoviral-mediated

94 Notch signaling was blocked with the gamma-secretase inhibitor dibenzazepine (DBZ).

95 Furthermore, treatment with the gamma-secretase inhibitor dibenzazepine and neurogenin-3

96 locking the NOTCH signaling pathway with the gamma-secretase inhibitor dibenzazepine increased the nu

97 Treatment of mice with the gamma-secretase inhibitor dibenzazepine to diminish Notc

98 A gamma-secretase inhibitor did not affect AChE transcript

99 se inhibition of gamma-secretase activity by gamma-secretase inhibitors did not affect the PEN-2 leve

100 mma-secretase components, and that selective gamma-secretase inhibitors differentially affect the tra

101 Mice were also given the gamma-secretase inhibitor difluorophenacetyl-l-alanyl-S-

102 y, treatment of wild-type splenocytes with a gamma-secretase inhibitor directly promoted the granuloc

103 ckade of Notch signaling by dibenzazepine, a gamma-secretase inhibitor, disrupted the large vessels a

104 Our studies further show that gamma-secretase inhibitors do not adversely impact autop

105 Analysis with specific gamma-secretase inhibitors, dominant-negative gamma-secr

106 uire Notch1 mutations and are sensitive to a gamma-secretase inhibitor, endogenous Nras G12D/+ signal

107 Neurosphere cultures treated with gamma-secretase inhibitors exhibit a similar phenotype o

108 as independently inhibited by three specific gamma-secretase inhibitors, expression of the dominant n

109 In vitro, gamma-secretase inhibitors extinguished expression of No

110 Functional gamma-secretase inhibitors (FGSIs) can block the cleavag

111 Novel benzodiazepine-containing gamma-secretase inhibitors for potential use in Alzheime

112 has been performed with a range of selected gamma-secretase inhibitors from six distinct structural

113 stigated the combination between miR-34a and gamma-secretase inhibitor (gammaSI), Sirtinol or zoledro

114 Ex vivo, Gamma secretase inhibitor (GSI) (inhibitor of Notch rece

115 Gamma secretase inhibitors (GSI) block proteolytic activ

116 Treatment with a gamma-secretase inhibitor (GSI) alone induced apoptosis

117 Treatment with a novel sulfonamide-type gamma-secretase inhibitor (GSI) attenuated the formation

118 of mice carrying autochthonous NSCLCs with a gamma-secretase inhibitor (GSI) blocks cancer growth.

119 Inhibition of the Notch pathway with a gamma-secretase inhibitor (GSI) decreased both the Notch

120 -1 that produces NICD, we asked whether this gamma-secretase inhibitor (GSI) might prevent dendritic

121 t after training or before testing) with the gamma-secretase inhibitor (GSI) N-[N-(3,5-difluorophenac

122 activity was abrogated by a Notch inhibitor, gamma-secretase inhibitor (GSI) or Notch-1 small-interfe

123 Inhibition of Notch1 signalling with a gamma-secretase inhibitor (GSI) or Notch1 RNA interferen

124 locked in PCT cell lines by treatment with a gamma-secretase inhibitor (GSI) or transduction of a dom

125 over, pharmacologic Notch inhibition using a gamma-secretase inhibitor (GSI) rescued the hyperprolife

126 To understand the molecular basis of gamma-secretase inhibitor (GSI) sensitivity in breast ca

127 Treatment of T(EFF) cells with a gamma-secretase inhibitor (GSI) strongly inhibited Notch

128 We tested the effects of a gamma-secretase inhibitor (GSI) that blocks Notch signal

129 13 T-cell leukemia cell lines treated with a gamma-secretase inhibitor (GSI) to inhibit Notch signals

130 We used gamma-secretase inhibitor (GSI) to prevent the cleavage

131 acologic inhibition of Notch signaling using gamma-secretase inhibitor (GSI) treatment blocks (1) TGF

132 In contrast, gamma-secretase inhibitor (GSI), a Notch pathway inhibit

133 Treatment of CD4(+) T cells with a gamma-secretase inhibitor (GSI), which inhibits Notch si

134 nant-negative IGF-1R sensitized ACL cells to gamma-secretase inhibitor (GSI)-induced apoptosis.

135 her with cyclin D3 shows partial rescue from gamma-secretase inhibitor (GSI)-induced G(1) arrest in t

136 model to test the mechanisms of action of a gamma-secretase inhibitor (GSI).

137 Studies using gamma-secretase inhibitors (GSI and LY-411,575), which b

138 , we demonstrate that inhibition of Notch by gamma-secretase inhibitors (GSI) is efficacious in downs

139 ized that inhibition of Notch signaling with gamma-secretase inhibitors (GSI) may enhance the chemose

140 in many gliomas and can be suppressed using gamma-secretase inhibitors (GSI).

141 Gamma secretase inhibitors (GSIs) impair notch signaling

142 gamma-Secretase inhibitors (GSIs) are drugs used in rese

143 Notch/gamma-secretase inhibitors (GSIs) block proliferation an

144 Gamma-secretase inhibitors (GSIs) block the activation o

145 gamma-secretase inhibitors (GSIs) can block NOTCH recept

146 Targeting glioblastoma stem cells with gamma-secretase inhibitors (GSIs) disrupts the Notch pat

147 However, inhibition of NOTCH signaling with gamma-secretase inhibitors (GSIs) has shown limited anti

148 Although gamma-secretase inhibitors (GSIs) have progressed into t

149 that could synergize with or substitute for gamma-secretase inhibitors (GSIs) in T-cell acute lympho

150 nditionally deleting Notch1 or administering gamma-secretase inhibitors (GSIs) in vivo attenuated dis

151 Inhibiting Notch 3 activation in vitro with gamma-secretase inhibitors (GSIs) or small interfering R

152 ile of a novel spirocyclic sulfone series of gamma-secretase inhibitors (GSIs) related to MRK-560.

153 ouse or human T-ALL cell lines in vitro with gamma-secretase inhibitors (GSIs) results in growth arre

154 leukemia (T-ALL) led to clinical testing of gamma-secretase inhibitors (GSIs) that prevent NOTCH1 ac

155 sphere-like ReN cell aggregate cultures with gamma-secretase inhibitors (GSIs), but not SGSMs, induce

156 en we cultured utricles from young mice with gamma-secretase inhibitors (GSIs), striolar SCs complete

157 ociated with repeated exposure to functional gamma-secretase inhibitors (GSIs).

158 which is reversed by Notch1 inhibition with gamma-secretase inhibitors (GSIs).

159 astic leukemia (T-ALL) and Notch inhibitors (gamma-secretase inhibitors [GSIs]) have produced respons

160 These gamma-secretase inhibitors had no effect on enzymatic ac

161 Selective reduction of Abeta with a gamma-secretase inhibitor has no effect on the frequency

162 Progress toward clinical use of gamma-secretase inhibitors has, however, been hampered d

163 Therefore, different gamma-secretase inhibitors have been developed to reduce

164 The development of potent gamma-secretase inhibitors having substituted heterocycl

165 gamma-Secretase inhibitors hold promise for the treatmen

166 A negative drug trial with a broad spectrum gamma-secretase inhibitor in AD patients has severely da

167 The disruption of Notch signaling by a gamma-secretase inhibitor in an in vitro organ culture s

168 E1 or BACE2 was blocked by a number of known gamma-secretase inhibitors in a concentration-dependent

169 f systemic Notch blockade were observed with gamma-secretase inhibitors in preclinical and early clin

170 of novel therapies, including nelarabine and gamma-secretase inhibitors, in adult patients with T-cel

171 that whereas blocking Notch signaling with a gamma-secretase inhibitor increased the conversion of in

172 The absence or reduction of PS1, as well as gamma-secretase inhibitors, increases neuronal miR-212,

173 gamma-Secretase inhibitor-induced apoptosis of lung tumo

174 2 trafficking, PS1 was also required for the gamma-secretase inhibitor-induced plasma membrane accumu

175 Inhibition of Notch signaling by gamma-secretase inhibitor inhibited the proliferation an

176 In contrast to small-molecule gamma-secretase inhibitors, kinetic inhibition studies d

177 w that the new zeta-cleavage is inhibited by gamma-secretase inhibitors known as transition state ana

178 e Abeta aggregation inhibitor clioquinol and gamma-secretase inhibitor L-685,458 attenuated caspase-3

179 hemic hemisphere and that treatment with the gamma-secretase inhibitor L-685,458 improves the neurolo

180 profen (1 microM, 48 h) or with the specific gamma-secretase inhibitor L-685,458 significantly attenu

181 The gamma-secretase inhibitor L-685,458 significantly recons

182 The gamma-secretase inhibitor L-685458 significantly reconst

183 disruption of HUVEC-based tube formation by gamma-secretase inhibitor L1790 confirmed the critical r

184 sequences of gamma-secretase inhibition, the gamma-secretase inhibitor LY-411,575 was administered to

185 deed, we found that acute treatment with the gamma-secretase inhibitor LY-411575 reduces soluble Abet

186 Treatment with the gamma-secretase inhibitor LY3039478 led to inhibition of

187 dibenzazepinone 1, the core structure in the gamma-secretase inhibitor LY411575, can be prepared in f

188 These effects were suppressed by the gamma-secretase inhibitor LY450139.

189 asure Abeta production during treatment of a gamma-secretase inhibitor, LY450139.

190 Treatment of WT neuronal cultures with gamma-secretase inhibitor mimicked the loss of PS1, lead

191 The gamma-secretase inhibitor MRK-560 represents an exceptio

192 We demonstrate that the gamma secretase inhibitor MRK003 effectively inhibits in

193 enhanced by the combination of ATRA and the gamma-secretase inhibitor N-(N-(3,5-difluorophenacetyl)-

194 The effects of Notch inhibition, using the gamma-secretase inhibitor N-(N-[3,5-difluorophenacetyl]-

195 Treatment with the gamma-secretase inhibitor N-[N-(3,5-difluorophenacetyl)-

196 The gamma-secretase inhibitor N-[N-(3,5-Difluorophenacetyl-L

197 mbryonic fibroblast lines and blocked by the gamma-secretase inhibitors N-[N-(3,5-difluorophenacetyl-

198 treatment with the notch pathway inhibitor (gamma-secretase inhibitor), N-S-phenyl-glycine-t-butyl e

199 vation to hypoxia tolerance using a specific gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)

200 Pretreatment with the gamma-secretase inhibitor, N-[N-(3,5-difluorophenacetyl)

201 tured mouse metanephroi in the presence of a gamma-secretase inhibitor, N-S-phenyl-glycine-t-butyl es

202 ion of amyloid-beta generation with beta- or gamma-secretase inhibitors not only decreased amyloid-be

203 N2a neuroblastoma cells exposed to beta- or gamma-secretase inhibitors, nuclear translocation was gr

204 ous other substrates, raising concerns about gamma-secretase inhibitor off-target effects.

205 this study was to determine the effects of a gamma-secretase inhibitor on the production of Abeta in

206 lar domain rescued the inhibitory effects of gamma-secretase inhibitors on VEGF-induced angiogenesis.

207 generate a new series of helical peptides as gamma-secretase inhibitors, one of which, 11, showed an

208 Notch was inhibited in culture with a gamma-secretase inhibitor or dominant negative mastermin

209 Cell cultures were treated with gamma-secretase inhibitor or GSM.

210 N1(IC) levels in MCF7/VP cells with either a gamma-secretase inhibitor or shRNA led to reduction of A

211 the Notch pathway by treatment with either a gamma-secretase inhibitor or stable expression of shRNA

212 nd that APP-PS1 interactions occur even when gamma-secretase inhibitors or "dominant-negative" PS1 mu

213 ls with the Notch activation signature using gamma-secretase inhibitors or by expressing a dominant n

214 Notch inhibition by gamma-secretase inhibitors or by using lentiviral mediat

215 By using pharmacological gamma-secretase inhibitors or cell lines lacking functio

216 Moreover, by inhibiting Notch signaling with gamma-secretase inhibitors or Notch receptor-specific ne

217 itizes them to inhibition via small-molecule gamma-secretase inhibitors or NOTCH-1 RNA interference.

218 Inhibition of Notch using gamma-secretase inhibitors or soluble Delta-like4-Fc dur

219 ived intravitreal injection of PEDF, DAPT (a gamma-secretase inhibitor) or PEDF + DAPT at the time of

220 jective response rate after therapy with the gamma-secretase inhibitor PF-03084014 in patients with r

221 ases were also seen after treatment with the gamma-secretase inhibitor PF-03084014.

222 ise, low betaCTF or C99 expression decreased gamma-secretase inhibitor potency.

223 ch pathway are the Notch receptors, in which gamma-secretase inhibitors prevent the generation of the

224 Moreover, exposure of the cells to a gamma-secretase inhibitor prevented Notch1 processing, d

225 A gamma-secretase inhibitor prevented the formation of a 1

226 Accordingly, gamma-secretase inhibitors prevented the EphB-induced sp

227 mice, the cleavage product from Ac-gamma-Glu-gamma-secretase inhibitor prodrug 13a (gamma-GT-targetin

228 mma-GCT-targeting) but not from Ac-alpha-Glu-gamma-secretase inhibitor prodrug 15a (APA-targeting) ac

229 ical inhibition of the Notch pathway (with a gamma-secretase inhibitor) protected rats with proteinur

230 Selective reduction of Abeta with a gamma-secretase inhibitor provided similar improvement,

231 Consistent with this hypothesis, gamma-secretase inhibitor radioligand occupancy studies

232 In this study, gamma-secretase inhibitor radioligands were used to eval

233 macological blockade of Notch signaling with gamma-secretase inhibitors raises insulin sensitivity af

234 ble by a photoactivated active site-directed gamma-secretase inhibitor rather than total PS1; hence,

235 trated that inhibition of Notch signaling by gamma-secretase inhibitors reduced tumor cell proliferat

236 Blockage of Notch4 processing to ICD4 by gamma-secretase inhibitor renders MCF-7 cells sensitive

237 that inhibition of Notch activation using a gamma-secretase inhibitor represents a potential new app

238 cing amyloid-beta by treating neurons with a gamma-secretase inhibitor restored surface expression of

239 with D283 medulloblastoma xenografts with a gamma secretase inhibitor resulted in decreased prolifer

240 hway inhibition with soluble Delta ligand or gamma secretase inhibitors resulted in a marked reductio

241 Treatment with a gamma-secretase inhibitor results in excess regenerated

242 ent manner, whereas Notch inhibition using a gamma-secretase inhibitor reversed this process.

243 ng Notch signaling, through injection of the gamma-secretase inhibitor RO4929097, stimulates a subset

244 The gamma-secretase inhibitor (S,S)-2-[2-(3,5-difluorophenyl

245 auma, when Notch signaling is inhibited by a gamma-secretase inhibitor selected for potency in stimul

246 vation of Notch transcriptional targets in a gamma secretase inhibitor-sensitive manner and causes No

247 Agonists at those receptors trigger gamma-secretase-inhibitor-sensitive biogenesis of Abeta4

248 Notably, a gamma-secretase inhibitor significantly blocked Notch-me

249 tion of Notch signaling in these cells using gamma-secretase inhibitors significantly delayed leukemo

250 Moreover, multiple gamma-secretase inhibitors significantly increased alpha

251 tch signaling, via knockdown of Notch1 or by gamma-secretase inhibitors, significantly reduced TGF-be

252 Treatment with DAPT, a gamma-secretase inhibitor, similarly interfered with the

253 We further showed that gamma-secretase inhibitors specifically accelerated the

254 1 and 2 (PS1/2) knockouts recapitulated the gamma-secretase inhibitor studies, as compared with thei

255 ing Ab or specific inhibition of Notch1 by a gamma-secretase inhibitor substantially inhibits LFA-1/I

256 In vivo, administration of gamma-secretase inhibitors substantially impeded TH1-med

257 Suppression of Notch signaling by gamma-secretase inhibitors substantially reduced cell co

258 IG2/LMO1 transgenic mice was suppressed by a gamma-secretase inhibitor, suggesting that Notch1 up-reg

259 r cells was counteracted by treatment with a gamma-secretase inhibitor, suggesting that the aggressiv

260 ehavior of APP after treatment with beta- or gamma-secretase inhibitors suggests that the amount of b

261 /R injury activated Notch-2 signaling, and a gamma-secretase inhibitor suppressed I/R-induced Notch-2

262 nally, inhibition of Notch signaling using a gamma-secretase inhibitor suppressed proliferation of Ts

263 y, targeting Notch signaling with a peptidyl gamma-secretase inhibitor suppressed survivin levels, in

264 lates Notch signaling, and administration of gamma-secretase inhibitors suppressed the intestinal dys

265 Potential nephroprotective effects of the gamma-secretase inhibitor targeted prodrugs were investi

266 nyl]-S-phenylglycine t-butyl ester (DAPT), a gamma-secretase inhibitor that blocks activation of Notc

267 alpha-secretase in generating an endogenous gamma-secretase inhibitor that down-regulates the produc

268 MRL631, a gamma-secretase inhibitor that is unable to penetrate th

269 Semagacestat is a small-molecule gamma-secretase inhibitor that was developed as a potent

270 for the development of clinically effective gamma-secretase inhibitors that can reduce amyloid-beta

271 o activated transcription in the presence of gamma-secretase inhibitors that prevent amyloid beta-pep

272 In the presence of gamma-secretase inhibitor, the antitumor cytolytic abili

273 ated by Notch signaling; administration of a gamma-secretase inhibitor to mice increased the number o

274 Thus, using gamma-secretase inhibitors to modulate Notch signaling m

275 eatment with a series of chemically distinct gamma-secretase inhibitors to prevent Notch-1 signaling.

276 The use of specific gamma-secretase inhibitors to study the accumulation of

277 udy, we determined the ability of MRK-003, a gamma-secretase inhibitor, to inhibit Notch3 signaling,

278 e NF-kappaB subunit c-Rel was compromised in gamma-secretase inhibitor-treated and CSL/RBP-Jkappa KO

279 gamma-Secretase inhibitor treatment also increased endog

280 s harboring FBW7 mutations were resistant to gamma-secretase inhibitor treatment and this resistance

281 ages from CSL/RBP-Jkappa KO mice phenocopied gamma-secretase inhibitor treatment for reduced IL-12p40

282 growth arrest and apoptosis associated with gamma-secretase inhibitor treatment or Notch1 inhibition

283 Remarkably, in 2 mice, gamma-secretase inhibitor treatment reduced LIC frequenc

284 trategies to block NOTCH pathway activation: gamma-secretase inhibitor treatment, preventing nuclear

285 primary lymphoblasts were hypersensitive to gamma-secretase inhibitor treatment, which is known to i

286 ry cortical neurons, and can be prevented by gamma-secretase inhibitor treatment.

287 Gamma-secretase-inhibitor treatment prevents NOTCH1 nucl

288 gamma-secretase in terms of sensitivity to a gamma-secretase inhibitor, upregulation of Abeta42 produ

289 Using cell aggregation assays and gamma-secretase inhibitors we show that Wry is a novel N

290 ase cleavage site and Compound E, a specific gamma-secretase inhibitor, we found high levels of gamma

291 presenilin selectivity of several classes of gamma-secretase inhibitors, we observed that sulfonamide

292 S were made into one eye and either Abeta or gamma-secretase inhibitor were injected into their oppos

293 ibited at the G(1) phase by treatment with a gamma-secretase inhibitor which specifically blocks the

294 our strategy to design metabolically stable gamma-secretase inhibitors which are selective for inhib

295 We found that a gamma-secretase inhibitor, which functions opposite that

296 eceptor a promising target for drugs such as gamma-secretase inhibitors, which block a proteolytic cl

297 east cancer subtype and can be suppressed by gamma-secretase inhibitors, which effectively block rece

298 quitin ligase activity, or by treatment with gamma-secretase inhibitors, which prevent intramembrane

299 development of a new generation of selective gamma-secretase inhibitors with an improved side effect

300 henylglycine t-butylester (DAPT), a specific gamma-secretase inhibitor, would alter beta2-mediated ce