ライフサイエンスコーパス: U0126

1 (SB431542 or LY364947) or ERK1/2 (PD98059 or U0126)].

2 emistry, and activity was inhibited by using U0126.

3 cells, but the translocation was blocked by U0126.

4 given intra-LA infusion of the MEK inhibitor U0126.

5 l Pkd1 model of ADPKD using MEK1/2 inhibitor U0126.

6 nase inhibitor, but not by the MEK inhibitor U0126.

7 , which could be neutralized by BAPTM/AM and U0126.

8 sed by treating cells with the MEK inhibitor U0126.

9 ase (MEK) was inhibited by the MEK inhibitor U0126.

10 e mutants are sensitive to the MEK inhibitor U0126.

11 TAT3, which were inhibited by treatment with U0126.

12 ially affected in eggs matured in vitro with U0126.

13 K1/2 phosphorylation by the MEK1/2 inhibitor U0126.

14 en-activated protein kinase ERK1/2 inhibitor U0126.

15 ignificantly inhibited by preincubation with U0126.

16 cells, an effect that could be abolished by U0126.

17 This promitotic effect was eliminated by U0126.

18 ctivated protein kinase (MAPK)/ERK inhibitor U0126.

19 e mitogen-activated protein kinase inhibitor U0126.

20 MDDCs upon exposure to the MEK1/2 inhibitor U0126.

21 rmalized by administration of MAPK inhibitor U0126.

22 were also completely blocked by LY294002 or U0126.

23 were markedly reduced by the MAPK inhibitor, U0126.

24 ivated protein/ERK kinase-specific inhibitor U0126.

25 utralizing aptamers or the MEK/ERK inhibitor U0126.

26 ], whereas PAR2 effects were only blocked by U0126.

27 of p53 is sensitive to the MEK/ERK inhibitor U0126.

28 nhibition of basal pERK1/2 (vehicle AUC with U0126 0.60 +/- 0.30).

29 (mitogen-activated protein) kinase inhibitor U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-amino-phenylthi

30 plication of the MAP kinase kinase inhibitor U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-amino-phenylthi

31 n, or the MAP kinase kinase (MEK) inhibitor, U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio

32 ar signal-regulated kinase kinase inhibitor, U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio

33 vated protein kinase (MEK)/ERK1/2 inhibitor, U0126 (1.0 mug/0.5 mul/hemisphere), microinfused bilater

34 lopropylmethoxy-3,4-difluoro-benzamide], and U0126 [1,4-diamino-2,3-dicyano-1,4-bis(2-aminophynylthio

35 ation of the MAP kinase kinase 1/2 inhibitor U0126 [1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenylmerc

36 d pMF was abolished by the MEK/ERK inhibitor U0126 [1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenylmerc

37 pMF was attenuated by the MEK/ERK inhibitor U0126 [1,4-diamino-2,3-dicyano-1,4-bis(o-aminophenylmerc

38 SB415286 or U0126 (10 microM) suppression of Erk1/2 phosphorylation

39 EK)/ERK and PKA pathways by a combination of U0126 (10 micromol/L) and H-89 (5 micromol/L) reduced mo

40 (10(-10)-10(-7) M) or the ERK 1/2 inhibitor U0126 (10(-9)-10(-6) M) before incubation with Ad-myr-PK

41 M), p38 MAPK (SB203580, 10 muM), and ERK1/2 (U0126, 10 muM) resulted in down-regulation of IL-6-induc

42 U0126 (100 nM, 5 microM and 250 microM) significantly at

43 ERK1/2 inhibitors (AG1478, 10 mg/kg/day and U0126, 400 mug/kg/day, respectively) for 3 weeks.

44 Na+ current, in a manner similar to that of U0126 (a pharmacologic inhibitor of ERK signaling).

45 In addition, U0126 (a selective inhibitor of MEK kinase responsible f

46 roximity ligation assay and was abolished by U0126, a MAP kinase inhibitor.

47 lls treated with TGFbeta, and treatment with U0126, a MAP/Erk kinase (MEK) inhibitor, blocked the EMT

48 vasion in Np-1-overexpressing cells, whereas U0126, a MAP/extracellular signal-regulated kinase kinas

49 APK by silencing ERK1/2 or by treatment with U0126, a MAPK inhibitor, partially blocked the escalatio

50 U0126, a MEK inhibitor, had a moderate antiproliferative

51 using either recombinant ERK phosphatase or U0126, a MEK inhibitor, prevents accumulation of GFP-PCN

52 1396, a Ca(2+)-sensitive PYK2 inhibitor, and U0126, a MEK/ERK inhibitor.

53 ed by the PKC activator PMA and inhibited by U0126, a MEK1 inhibitor.

54 Addition of U0126, a specific antagonist of MEK, the enzyme that pho

55 Inhibition of ERK activation with U0126, a specific ERK inhibitor, significantly reduced v

56 fect was abolished by treating the mice with U0126, a specific ERK pathway inhibitor, showing that, i

57 itor staurosporine, and partially reduced by U0126, a specific inhibitor for ERKs.

58 Since U0126, a specific inhibitor for MEK1/2, also induced a p

59 rkedly inhibited in PK-15 cells treated with U0126, a specific inhibitor for MEK1/2/ERK1/2, whereas M

60 The treatment of cells with U0126, a specific inhibitor of ERK activation, resulted

61 Induction of Jag1 was efficiently blocked by U0126, a specific inhibitor of MAPK/ERK signaling, indic

62 etaRII/Fc chimera, a TGF-beta antagonist, or U0126, a specific MEK inhibitor, could significantly del

63 Also, U0126, a specific MEK inhibitor, was able to protect PC-

64 MEK inhibitor U0126 abolished nicotine-induced rise in P-ERK1/2, but n

65 Inhibition of MEK activity with U0126 abolished phosphorylation of both NHE1 and p90(RSK

66 U0126 abolished REOX-induced elevation and translocation

67 n-activated protein kinase kinase (MEK) with U0126 abolished VWF-induced platelet aggregation and thr

68 ing the ERK pathway, as the ERK1/2 inhibitor U0126 abolishes the increase in expression of CRC cell s

69 binding, and inhibition of ERK activity with U0126 abrogated the loss of water uptake following OGD.

70 002, rapamycin) but not the MEK/ERK pathway (U0126) abrogated laminin-mediated survival.

71 The MEK inhibitor, U0126, abrogated GEP production in response to ET-1 and

72 Treatment with a MEK1/2 inhibitor, U0126, abrogated the enhanced proliferation of the KCM c

73 tracellular regulated kinase (MEK) inhibitor U0126 acted to induce fibrosis and blocked the ability o

74 t depended on memory reactivation given that U0126 administered following exposure to a novel context

75 the MAPK/ERK1/2 (MEK1/2)-specific inhibitor U0126 all markedly attenuated IL-25-induced angiogenesis

76 and mitogen-activated protein kinase (MAPK; U0126) all showed dose-dependent suppression of the prol

77 rfusion increased infarct size compared with U0126 alone.

78 In the presence of ERalpha, U0126 also dramatically reduces (i) ligand-dependent col

79 cretion was not inhibited by MAPKK inhibitor U0126, although p42/p44 MAPK was phosphorylated.

80 SP1 enhanced TLR4 mediated ERK signaling and U0126 (an ERK inhibitor) blocked LPS induced beta3 integ

81 by MEKK1 siRNA, PD98059 (an MEK inhibitor), U0126 (an ERK inhibitor), and RSK1 siRNA.

82 lin-dependent protein kinase II (CaMKII) and U0126 [an extracellular signal-regulated protein kinase

83 The improved response was prevented by U0126, an Erk inhibitor.

84 Finally, the administration of U0126, an inhibitor of ERK activation, to infected mice

85 human Jurkat T cell line in the presence of U0126, an inhibitor of ERK activation.

86 U0126, an inhibitor of ERK kinase, or LY294002, an inhib

87 Only after intraperitoneal treatment of U0126, an inhibitor of ERK phosphorylation, was lens dev

88 mycin, an inhibitor of protein synthesis, by U0126, an inhibitor of MEK1/2 kinases, and by rapamycin,

89 rthermore, treatment of the mutant mice with U0126, an inhibitor of mitogen-activated protein (MAP) k

90 Intra-AcbC infusions of U0126, an inhibitor of the ERK kinase MEK, prevent both

91 Here we show that treatment with U0126, an inhibitor of the ERK2 upstream kinases MEK1/2,

92 U0126, an inhibitor of the mitogen-activated protein kin

93 hearts in the presence of the MEK inhibitor U0126 and found that U0126 induced intra-cardiac cartila

94 The MEK1/2 inhibitor U0126 and knockdown of MEK1/2 expression with small inte

95 U0126 and LY249002, specific inhibitors of MAPK/ERK kina

96 Pretreatment with U0126 and LY294002 decreased both pERK and pAkt in phren

97 pMEK1(in vitro) bound allosteric inhibitors U0126 and PD0325901 with a significantly lower affinity

98 he allosteric non-ATP-competitive inhibitors U0126 and PD0325901 with and without the nucleotide.

99 The non-ATP-competitive MEK1 inhibitors, U0126 and PD0325901, showed no preference for npMEK1 and

100 activated protein kinase 1 and 2 inhibitors U0126 and PD325901 rescues the Npr2(pwe/pwe) growth defe

101 In turn, MEK inhibitors U0126 and PD98059 and siRNA-mediated depletion of either

102 activating KRAS mutation; the MEK inhibitors U0126 and PD98059 elicit a similar response.

103 RIE-1 or ROSE cells with the MEK inhibitors U0126 and PD98059 increased Par-4 protein expression.

104 ERK1/2 activation via the MEK1/2 inhibitors U0126 and PD98059 results in decreased Stx1-mediated IL-

105 The MEK1/2 inhibitors U0126 and PD98059 reversed the protective effects of COL

106 activated protein kinase (MAPK) signaling by U0126 and PD98059 significantly reduced the UVR response

107 is inhibited by the MEK-specific inhibitors U0126 and PD98059, but not by the PI3K-specific inhibito

108 eatment of MEK1/2 kinase inhibitors, such as U0126 and PD98059, which inhibit the ERK1/2 activation a

109 mitogen-activated protein kinase inhibitors (U0126 and SB203580) were sufficient to block Nup hyperph

110 more, blockade of the ERK or JNK pathways by U0126 and SP600125, respectively, abolished ADP- and 2-M

111 GE2 and CM and this blockage was reversed by U0126 and the CM depleted of PGE2.

112 pathways using the MEK inhibitor PD184352 or U0126 and the PI3K/Akt inhibitor perifosine strikingly i

113 of the ERK1/2 signaling pathway, PD98059 and U0126 and the spleen tyrosine kinase (Syk) inhibitor, Pi

114 l score and histology did not differ between U0126 and vehicle-treated rats after cardiac arrest.

115 no-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126) and 2'-amino-3'-methoxyflavone (PD98059), had sim

116 879) and inhibitors of Trk-induced MAPK/Erk (U0126) and Akt kinase (LY294002) signaling, but not an i

117 nhanced the effects of both MAPK/ERK kinase (U0126) and broad spectrum PKC inhibitor (chelerythrine c

118 tracellular receptor kinase (ERK) inhibitor (U0126) and c-Jun N-terminal kinase (JNK) inhibitor (SP60

119 ginally toxic concentrations of PD184352 (or U0126) and dasatinib synergistically potentiated mitocho

120 acological MAPK inhibitors specific for MEK (U0126) and p38 (SB203580), but not JNK (SP600125).

121 ated by simultaneous treatment with the MEK (U0126) and PI3-K (LY294002) inhibitors.

122 Combined application of inhibitors of ERK (U0126) and PKA (KT5720) was necessary to block completel

123 enesis were MEK dependent (blocked by 10 muM U0126) and PKA independent (insensitive to 30 muM H-89 o

124 MEK/ERK pharmacologic inhibitors (PD98059 or U0126) and RNAi-induced depletion of N-Ras.

125 o-2,3-dicyano-1,4-bis(methylthio) butadiene (U0126)], and therefore cAMP-dependent target genes poten

126 organ culture studies with a Mek inhibitor, U0126, and a Fgf receptor inhibitor, SU5402, indicate th

127 GF receptor and to the inhibitors SU5402 and U0126, and a PKC pathway, which is dependent on the intr

128 demonstrated by inhibition of the pathway by U0126, and by BRAF RNA interference.

129 cer cell growth and resistance to gefitinib, U0126, and genotoxicity.

130 The MEK1/2 inhibitor, U0126, and mutation of the ERK-dependent phosphorylation

131 ells treated with MAPK kinase 1/2 inhibitors U0126, and PD98059 (IC(50) approximately 25 micromol/L).

132 ls was inhibited by manumycin A, BAY43-9006, U0126, and transfection with a dominant-negative Ras mut

133 eased after treatment with the MEK inhibitor U0126 as well as after knockdown of MEK1/2 by shRNA in H

134 MAPK/ERK kinase (MEK) inhibitors PD98059 and U0126, as well as by ADAM10 and -17 inhibitors.

135 Furthermore, similar to U0126, baclofen+muscimol-induced (B+M; 106.8/5.7 ng/0.5

136 ent, rats received intrathalamic infusion of U0126 before long-term potentiation (LTP)-inducing stimu

137 no-1,4-bis(o-aminophenylmercapto) butadiene (U0126) before fear conditioning.

138 Treatment with either U0126, beta-xyloside, or heparin resulted in a reduction

139 as/RAF/MEK/Erk signaling using MEK inhibitor U0126 blocked anchorage-independent growth in cells lack

140 inhibitor pertussis toxin and MEK inhibitor U0126 blocked C5a inhibition of LPS-induced IL-6 and TNF

141 FkappaB inhibitors and the MEK/ERK inhibitor U0126 blocked CLA-mediated IL-6 gene expression.

142 ivated protein kinase kinase (MEK) inhibitor U0126 blocked ouabain-induced ERK activation and cell pr

143 hibition of the MAPK pathway with PD98059 or U0126 blocked the DFMO-induced induction of p21 and the

144 in HepG2 human hepatoma cells by PD98059 or U0126 blocked the increased phosphorylation of eIF2alpha

145 The MAPK inhibitor, U0126, blocked MMP-1 activity and restored HGF-inhibited

146 aling by the MEK (MAPK/ERK kinase) inhibitor U0126 blocks bidirectional melanosome transport along mi

147 ced p27(kip1) down-regulation was blocked by U0126 but not by wortmannin.

148 n of HT-29 was inhibited by the treatment of U0126 but not in HeLa cells, and the treatment of HT-29

149 acellular-signal-regulated kinase) inhibitor U0126, but not by AKT (serine/threonine protein kinase A

150 e also reduced in in vitro-matured eggs with U0126, but not in those similarly treated after in vivo

151 The MEK1/2 specific inhibitor U0126, but not NFkappaB inhibitors, reduced basal Tspo p

152 The MAPK/ERK kinase (MEK)-1 inhibitor U0126, but not the p38-MAPK pathway inhibitor SB203580,

153 nd was significantly suppressed by 10 microM U0126, but was not affected by 10 microM of either SB203

154 calcium chelator BAPTM/AM and MEK inhibitor (U0126) can reverse Rap2B-induced ERK1/2 phosphorylation.

155 LT and the ERK1/2 pathway-specific inhibitor U0126 caused a decrease in major histocompatibility comp

156 HCT116 cells, inhibition with 30 micromol/L U0126 caused depletion of P-ERK1/2 and a decrease in pho

157 imatinib with LY294002 or rapamycin but not U0126 caused greater than additive increases in apoptosi

158 ive cells with BPDE and the MEK1/2 inhibitor U0126 caused little change in c-Jun and COX-2 expression

159 a PI3K inhibitor plus the MEK/ERK inhibitor U0126 completely eliminated inhibition by NGF.

160 ent of melanoma cells with the MEK inhibitor U0126 decreased NF-kappaB binding to its DNA recognition

161 fic MEK1/2 inhibitors, flavenoid PD98059 and U0126, decreased the basal and TGF-beta1-stimulated Vp-1

162 ce or by using the MEK1/2-specific inhibitor U0126 delayed the passage of synchronized HeLa cells int

163 r reduced infarct size, while combination of U0126 delivered at ischemia onset with psi deltaRACK inj

164 ERK and CREB phosphorylation was blocked by U0126, demonstrating that ERK/MAPK activation mediated t

165 In contrast, U0126 dephosphorylated ERK1/2 and increased nuclear CAR

166 Bath application of the MEK1/2 inhibitor U0126 did not alter leptin-induced suppression of AMPAR

167 on and spatial memory, but the ERK inhibitor U0126 did not.

168 Treatment of cells with a MEK1/2 inhibitor, U0126, dramatically reduced the phosphorylation of ERK,

169 y injection of the MAPK/ERK kinase inhibitor U0126 during pregnancy.

170 9 in a manner identical to the ERK inhibitor U0126: either inhibitor occluded the effect of the other

171 Inhibition of ERK1/2 signaling using U0126 enhanced HIF-1alpha stabilization, implicating ERK

172 cells, and the treatment of HT-29 cells with U0126 enhanced radiation sensitivity possibly due to the

173 ity, and pretreatment with the MEK inhibitor U0126, ERK1/2 inhibitor PD98059, or small interference R

174 The restoration of c-Jun in U0126-exposed cells was associated with increased c-Jun

175 ein rebounded to normal levels 4 h following U0126 exposure but not after LT exposure.

176 tment of MDA-MB-231 cells with 50 micromol/L U0126 for 2, 4, 8, 16, 24, 32, and 40 hours caused inhib

177 st, the lower concentration of 10 micromol/L U0126 for 40 hours had no significant effect on either P

178 and SB202190 for p38, SP600125 for JNK, and U0126 for ERK) or NFkappaB pathways (MG-132 and SC-514).

179 ow dose of irradiation, and indomethacin and U0126 further enhanced this effect.

180 Smad3-deficient cells with the MEK inhibitor U0126 further reduced cell survival but not migration.

181 d gene transcription, which was inhibited by U0126, GF109203, and calcium chelators.

182 n of basal MEK-ERK activity with PD98059 and U0126 had little effect.

183 f inflammation, whereas the MEK1/2 inhibitor U0126 had no effect and the flavonoid apigenin, a nonspe

184 ibronectin, whereas inhibition of MEK/ERK by U0126 had no effect.

185 MA expression was reduced by MEK inhibition (U0126); however, the levels of pERK, pSmad3, or the exte

186 Findings revealed that thalamic infusion of U0126 impaired LTP in the LA.

187 Relative to vehicle controls, infusion of U0126 impaired training-induced increases in Arc/Arg3.1

188 dification was blocked by the MEK1 inhibitor U0126, implying that extracellular signal-regulated kina

189 -activated protein kinase kinase 1 inhibitor U0126 in alpha7 integrin-deficient VSMCs suppressed extr

190 itivity between Taxol and the MEK inhibitor, U0126 in human cancer cell lines.

191 EGFR inhibitor AG1478 and the MEK inhibitor U0126 in rat and human cultured goblet cells.

192 MDA-MB-435 cells treated with PD98059 or U0126 in the presence and absence of DFMO exhibited a ma

193 e (PI3K) by Ly294002 or inhibition of ERK by U0126 in vivo abolished CpG-ODN attenuation of CLP-induc

194 Confirming this, the ERK1/2 inhibitor U0126 increased sensitivity to CP.

195 891A) in NIH-3T3 cells was also inhibited by U0126, indicating a role of the ERK1/2 pathway in RET-me

196 protein phosphatase PP2A, and Mek-inhibitor U0126, indicative of phosphorylation-dependent regulatio

197 ce of the MEK inhibitor U0126 and found that U0126 induced intra-cardiac cartilage formation, suggest

198 not the MAP/ERK kinase inhibitors PD98059 or U0126 induced the nuclear translocation of apoptosis-ind

199 Moreover, the occurrence of U0126-induced migratory inhibition coincided with slug r

200 In contrast, intra-NAcc U0126 infusion had no effect on rats' food-reinforced in

201 U0126 inhibited Ad-myr-PKCalpha-stimulated proliferation

202 A dose of 100 mug U0126 inhibited ERK bilaterally for 12 to 24 h and decre

203 Treatment with U0126 inhibited migration in both conditions, demonstrat

204 tion by Th1 cells, whereas the ERK inhibitor U0126 inhibited Th2 cell S1P-directed migration.

205 Inhibition of MEK1/2 by U0126 inhibited the induction of ER stress response gene

206 Inhibition of ERK1/2 by 1 microm U0126 inhibited zint-beta(2)-AR stimulation of I(Ca,L) i

207 tably, genetic (MEK1 silencing) or chemical (U0126) inhibition of ERK signaling restored constitutive

208 Pharmacological (U0126) inhibition, as well as virus-mediated downregulat

209 U0126 (inhibitor of mitogen-activated protein kinase/ext

210 Treatment with the MEK inhibitor U0126 inhibits ERK activation and decreases Notch and be

211 Additionally, treatment with U0126 inhibits the Rta-induced autophagy and the express

212 uced infarct size compared with vehicle, but U0126 injected at the onset of reperfusion had no protec

213 The ERK1/2 inhibitor, U0126, injected at ischemia onset, attenuated the increa

214 Finally, combination of U0126 injection at ischemia onset plus deltaV1-1 injecti

215 ard-seeking, we infused an inhibitor of ERK, U0126, into the NAcc before assessing rats' instrumental

216 lts show that MAPK signaling inhibition with U0126 is associated with a time-dependent decrease in ce

217 hibiting hemin-induced ERK-1/2 activation by U0126 (MAPK-inhibitor), the antioxidant N-acetyl cystein

218 The U0126-mediated inhibition of ERK1/2 activation impaired

219 c inhibitor), LY294002 (PI3K inhibitor), and U0126 (MEK inhibitor).

220 gative Akt, wortmannin (PI3K inhibitor), and U0126 (MEK inhibitor).

221 The inhibitors U0126, MIIC and PD98059 caused NAD(H) reduction, heme ox

222 ivated protein kinase kinase (MEK) inhibitor U0126 mimics the erlotinib results.

223 se, TrxR, or HIF-1 and by oxamate, apocynin, U0126, N-acetylcysteine, dithioerythritol, and antibodie

224 no-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126) of an HGF downstream kinase mitogen-activated pro

225 tivity and partially relieved the effects of U0126 on pancreatic cancer cell cycle arrest.

226 tion of p38 with SB203580 or ERK with either U0126 or a transfected dominant negative MEK did not int

227 Wortmannin/U0126 or AG490 was used for pharmacological RISK or SAFE

228 hr or 14 days after intra-AcbC infusions of U0126 or another MEK inhibitor, PD98059, CPP retrieval a

229 ion of ERK2 activity by the MEK1/2 inhibitor U0126 or by small interfering RNA silencing decreases MK

230 Posttraining infusion of either U0126 or DRB significantly impaired long-term retention

231 Moreover, neuroprotection was observed with U0126 or genetic ablation or pharmacological inhibition

232 eam of TLR2 by pharmacologic inhibition with U0126 or genetic deletion of Tpl2 blocks IL-10 secretion

233 Akt hyperactivation, reduced sensitivity to U0126 or LY294002, and ER-alpha hyperphosphorylation in

234 Only eNOS(s1179) was sensitive to U0126 or PTIO.

235 P-gammaS with compound 1 and ADP with either U0126 or the MEK1 clinical candidate PD325089 at 1.8, 2.

236 even in the presence of the MEK1/2 inhibitor U0126 or the PI3K inhibitor LY294002.

237 tion following preconditioning ischemia with U0126 or using the nonphosphorylatable 3ABim reduced the

238 As targeting BDNF or TrkB mRNA, and MEK/ERK (U0126) or PI3 kinase/Akt (PI828) inhibitors.

239 Treatment of cells with a MEK inhibitor (U0126) or proteasome inhibitor (epoxomicin) also up-regu

240 -treatment with the MAPK specific inhibitor (U0126) or the adenylate cyclase inhibitor dideoxyadenosi

241 g RNA (siRNA), specific inhibitors (PD98059, U0126), or siRNAs for MEK1/2.

242 Pretreatment with the MAPK inhibitor, U0126, or the LPS antagonist, polymyxin B, resulted in a

243 ated protein kinase phosphorelay modules, by U0126 partially reversed the IFNG-induced cytotoxicity i

244 MAPK/ERK kinase 1 and 2 (MEK1/2) inhibitor (U0126), partially blocked by a p38 inhibitor (SB202190),

245 owever, treatment with the MEK1/2 inhibitors U0126, PD184352 or the novel clinical candidate AZD6244

246 JNK, and AKT is inhibited, respectively, by U0126, PD98059 (mitogen-activated protein kinase kinase

247 nhibitors of the downstream kinases MEK-ERK (U0126, PD98059).

248 ment with TGFbeta1, ethanol, and PD98059 (or U0126) plus ethanol.

249 Inhibition of ERK1/2 with U0126 potently suppressed gAcrp-stimulated Egr-1 promote

250 Additionally, U0126 pretreatment at ischemia onset reduced infarct siz

251 inase inhibitor (K252a) or ERK1/2 inhibitor (U0126) pretreatment, and by knocking down Egr-1.

252 Inhibition of MEK1 by U0126 prevented phosphorylation of Bad at Ser112.

253 Inhibition of the second peak with U0126 prevented proliferation.

254 treatment with the ERK1/2-specific inhibitor U0126 prevented these galanin-induced effects.

255 n of GFP-PCNA in the zygote nucleus and that U0126 prevents incorporation of [3H]-thymidine into DNA.

256 t Clozapine, N-desmethylclozapine, DETC, and U0126 protect PC-12 cells by blocking the cell-type spec

257 o the MEK1/2-specific inhibitors PD98059 and U0126 protected both KSR+/+ and KSR-/- MEFs cells from C

258 Meanwhile, an MEK inhibitor (U0126) recovered sox2 and ngn1 transcript levels in cdk1

259 togen-activated protein kinase activation by U0126 reduced Bim ubiquitination and Bim degradation and

260 ibition of MEK1/2 activity using PD98059 and U0126 reduced Fra-1 expression, DNA binding, MMP-9 promo

261 ivated protein kinase kinase (MEK) inhibitor U0126 reduces surface expression of MHCI without affecti

262 eatment of obese mice with the ERK inhibitor U0126 rescued Baf60c and Deptor expression in skeletal m

263 itors for PI 3-kinase (LY294002) and MEK1/2 (U0126), respectively.

264 kinase (MEK) (bisindolyl maleimide (BIM) or U0126, respectively) blocked both PMA-induced Elk-1 tran

265 that inhibition of ERK1/2 phosphorylation by U0126 resulted in a decreased phosphorylation of PLCgamm

266 wounds in these mice with the MEK inhibitor U0126 resulted in a delay in wound healing suggesting th

267 or inactivation of ERK by the MEK inhibitor U0126 resulted in a precipitous decline in Mps1 levels.

268 p38 and ERK pathway inhibitors SB203580 and U0126 reversed the repressive effect of IL-17 on CXCL10

269 g during cue presentation, rats infused with U0126 showed a profound impairment in cue-induced instru

270 e-3-kinase/Akt (with LY294002) and ERK (with U0126) signaling, as well as short interfering RNA-media

271 (mitogen-activated protein kinase) inhibitor U0126 significantly attenuated the enhanced liver damage

272 Inhibiting MEK/ERK with U0126 significantly reduced expression of a cohort of pr

273 ancer cells; furthermore, the MEK2 inhibitor U0126 significantly reduces the tRNA-MEK2 interaction.

274 ly, we noticed that a 48-hour treatment with U0126 [specific mitogen-activated protein/ERK kinase (ME

275 ion of pERK by the pharmacological inhibitor U0126 specifically blocks KLF5-induced MKP-1 phosphoryla

276 n increase, while treatment with PD98059 and U0126, specifically blocked ERK phosphorylation, but had

277 or FTI-277 and MEK1/2 inhibitors PD98059 and U0126 strongly inhibited JSRV transformation of NIH 3T3

278 vity after fertilization with MEK inhibitor, U0126, substantially reduces the early peak of cdk2 acti

279 Therefore, a dose of U0126 sufficient to inhibit biochemical markers of ERK s

280 Inhibition of ERK activity by U0126 suppressed DV-induced expression and secretion of

281 The effects of the MEK/ERK inhibitor U0126, the heparan sulfate side chain formation inhibito

282 diate posttraining intrathalamic infusion of U0126, the mRNA synthesis inhibitor 5,6-dichloro-1-beta-

283 Relative to controls, U0126-treated cells showed constitutive decreases in pho

284 ylation levels of Thr-38 of CAR decreased in U0126-treated Huh-7 cells.

285 Combination of U0126 treatment and Fra-1/c-Jun knockdown did not yield

286 U0126 treatment had no effect on progression of cyst for

287 ic RNA transcription, were diminished during U0126 treatment of monolayers.

288 migration was not significantly inhibited by U0126 treatment or Fra-1/c-Jun silencing in cells expres

289 owed elevated phosphorylation in response to U0126 treatment, suggesting differential regulation of t

290 , which was also prevented by wortmannin and U0126 treatment.

291 educed in the presence of either PD 98059 or U0126, two compounds capable of blocking ERK1 and ERK2 p

292 Although U0126 up-regulated exogenous wild-type PML levels, it di

293 ition of outgrowth by LY294002, SR13668, and U0126 was reversible.

294 g the protein kinase inhibitors SB203580 and U0126, we also show that the ERK and p38 pathways regula

295 Using the MKK1/2 inhibitor U0126, we further show that MKK1/2-Erk1/2 pathway inacti

296 no-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126)], whereas PAR2 effects were only blocked by U0126

297 no-2,3-dicyano-1,4-bis(methylthio)butadiene (U0126), which blocks the phosphorylation of ERK.

298 y LY294002 and SR13668, but downregulated by U0126, which also abolished phosphorylation of p44/42 mi

299 n-activated protein kinase kinase inhibitor, U0126, which indicates the dependence on the mitogen-act

300 JNK is not inhibitable by the MEK inhibitor, U0126, while activation of raf, MEK, and ERK are blocked