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

10 to a biotinylated, benzophenone-derivatized 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 ich is abrogated by combination therapy with gamma secretase inhibitors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 gh track-density areas that are sensitive to gamma-secretase inhibitors.

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

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

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

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

35 ebrile Th2 switch was IL4 independent, but a gamma-secretase inhibitor abrogated it, and it was not f

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

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

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

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

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

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

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

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

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

45 Together, with the use of gamma-secretase inhibitors and scRNA-Seq, confirms that

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

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

48 gamma-secretase inhibitors are commonly used to probe NO

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

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

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

52 udies highlight the potential application of gamma-secretase inhibitors as a therapeutic target in pe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Unexpectedly gamma-secretase inhibitors can increase the secretion of

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

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

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

71 gamma-Secretase inhibitors confirmed that enzymatic acti

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

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

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

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

76 Pharmacological inhibition of Notch1 by gamma-secretase inhibitor DAPT (N-[N-(3,5-Difluorophenac

77 Blocking Notch receptor activation with the gamma-secretase inhibitor DAPT (N-[N-(3,5-difluorophenac

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

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

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

81 Using gamma-secretase inhibitor DAPT to acutely block canonica

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

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

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

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

86 ADAM10 inhibitor (GI254023X) and gamma-secretase inhibitor (DAPT) were used to inhibit CD

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 vels, and chronic Notch blockade through the gamma-secretase inhibitor dibenzazepine down-regulated L

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

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

99 ne tissues from mice given injections of the gamma-secretase inhibitor dibenzazepine, and mice with i

100 A gamma-secretase inhibitor did not affect AChE transcript

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

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

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

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

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

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

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

108 ombined with intrahippocampal injection of a gamma-secretase inhibitor evaluates the impact of Abeta

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

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

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

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

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

114 Gamma secretase inhibitors (GSI) block proteolytic activ

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

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

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

118 d resistant CCA cell lines pretreated with a gamma-secretase inhibitor (GSi) cocktail demonstrated th

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 Gamma-secretase inhibitors (GSI) and anti-Notch4 were al

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

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

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

142 Gamma secretase inhibitors (GSIs) impair notch signaling

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 nds and receptors, as well as small-molecule gamma-secretase inhibitors (GSIs), have been developed t

158 We have recently reported that clinical gamma-secretase inhibitors (GSIs), initially developed t

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

160 In search of novel gamma-secretase inhibitors (GSIs), we screened a series

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

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

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

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

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

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

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

168 gamma-Secretase inhibitors hold promise for the treatmen

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

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

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

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

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

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

175 MPTP opening was directly regulated by gamma-secretase inhibitors independent on organelle calc

176 gamma-Secretase inhibitor-induced apoptosis of lung tumo

177 2 trafficking, PS1 was also required for the gamma-secretase inhibitor-induced plasma membrane accumu

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

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

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

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

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

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

184 The gamma-secretase inhibitor L-685458 significantly reconst

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 Moreover, multiple gamma-secretase inhibitors significantly increased alpha

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

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

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

253 1 and 2 (PS1/2) knockouts recapitulated the gamma-secretase inhibitor studies, as compared with thei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 gamma-Secretase inhibitor treatment also increased endog

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

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

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

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

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

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

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

285 Gamma-secretase-inhibitor treatment prevents NOTCH1 nucl

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

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

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

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

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

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

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

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

294 nyl]-S-phenylglucine t-butyl ester (DAPT), a gamma-secretase inhibitor, which inhibits Notch signalin

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

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

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

298 se methods, the most common of which are the gamma-secretase inhibitors, which produce a pan-Notch in

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