ライフサイエンスコーパス: PD98059

1 wortmannin or PP2 (but not by MEK inhibitor PD98059).

2 mino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059).

3 on (KT5720), and MEK1/2 inhibition (U0126 or PD98059).

4 rs of the downstream kinases MEK-ERK (U0126, PD98059).

5 2 silencing or treatment with MEK inhibitor, PD98059.

6 and a pharmacologic MEK-specific inhibitor, PD98059.

7 NF, which were reversed by the MEK inhibitor PD98059.

8 the absence or presence of the MEK inhibitor PD98059.

9 ncy or by the addition of the Mek inhibitor, PD98059.

10 c changes were also blocked by SR141716A and PD98059.

11 iferase activity that was totally blocked by PD98059.

12 of EGFR antagonist AG1478 and MEK1 inhibitor PD98059.

13 this effect was inhibited by MEKK1 siRNA and PD98059.

14 MAPK) pharmacologic antagonists SB203580 and PD98059.

15 ion, which was blocked by the MEK inhibitor, PD98059.

16 rtmannin, or with the ERK pathway inhibitor, PD98059.

17 alpha siRNA but not by the MEK/ERK inhibitor PD98059.

18 he AR antagonist Casodex and MEK-1 inhibitor PD98059.

19 e mitogen-activated protein kinase inhibitor PD98059.

20 e following treatment with the MEK inhibitor PD98059.

21 at are prevented by intrathecal injection of PD98059.

22 ere unaffected by the MAPK ERK-1/2 inhibitor PD98059.

23 of ErbB-2 was inhibited by an MEK inhibitor, PD98059.

24 as blocked (P < 0.0001) by the ERK inhibitor PD98059.

25 rase, PP2, LY294002, and wortmannin, but not PD98059.

26 ded NOS3 up-regulation and were inhibited by PD98059.

27 ment, was restored by the MEK-1/2 inhibitor, PD98059.

28 ibited by ODQ and TEA but was insensitive to PD98059.

29 af-1 kinase inhibitor and the MEK inhibitor, PD98059.

30 bolished following local ERK inhibition with PD98059 (1 mug) and (ii) associated with significant red

31 ) in a manner inhibitable by a MEK inhibitor PD98059 (10 micromol/L), the antioxidant N-acetyl-l-cyst

32 Moreover, PD98059 (2'-amino-3'-methoxyflavone)-, PD184352- [2-(2-c

33 protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059 [2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-o

34 lar signal-regulated kinase kinase inhibitor PD98059 [2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-o

35 M with two structurally distinct inhibitors, PD98059 (30 microM) or UO126 (3 microM), inhibited the a

36 ing mAb (5 microg/mL), SP600125 (30 microM), PD98059 (40 microM), SB202190 (20 microM), or doxycyclin

37 PD98059 (5 micromol/L) also reduced MAPK activity and in

38 amino-3-methoxyphenyl-4H-1-benzopyran-4-one (PD98059) (50 microm) a specific inhibitor of mitogen-act

39 and interrupting this signaling either with PD98059, a chemical inhibitor of MEK, or by transfecting

40 sphorylation in goblet cells (P < 0.05), and PD98059, a MAPK/ERK kinase inhibitor, attenuated IL-33-s

41 Ser(795) phosphorylation could be blocked by PD98059, a MEK inhibitor, and greatly attenuated by apig

42 ion of K457A-PYK2 mutant or the treatment of PD98059, a MEK inhibitor.

43 Addition of PD98059, a MEK-1 inhibitor, suppressed ERK activation an

44 However, application of PD98059, a Mek/MAPK inhibitor, significantly enhanced os

45 PD98059, a mitogen-activated protein/extracellular-signa

46 uced the phosphorylation at Ser-293, whereas PD98059, a potent MAPK/ERK inhibitor, did not.

47 ycolic acid polymer chemically conjugated to PD98059, a selective MAPK inhibitor.

48 induced by E2 was significantly inhibited by PD98059, a specific ERK inhibitor, or by dominant negati

49 PD98059, a specific inhibitor of MEK1, almost completely

50 PD98059, a specific MEK inhibitor, significantly inhibit

51 Unlike PD98059, a widely-used MEK1/2 inhibitor, we found that P

52 The pharmacological inhibitor of ERK, PD98059, abrogated Fas-promoted cell survival in FADD kn

53 Neither ERK1/2 inhibitor PD98059 alone nor PD98059 combined with LY37 treatment i

54 Intrathecal PD98059 also attenuates capsaicin-induced secondary mech

55 ular signal-regulated kinase MAPK pathway by PD98059 also enhanced TRO's effects on GADD45 and apopto

56 PD98059 also increased back the expression of the MAD2 c

57 acellular signal-regulated kinase (ERK)-1/2, PD98059 also inhibits the more recently identified neuro

58 activity in vitro, whereas MEK1/2-inhibitor (PD98059) also blocked increases in MEK1/2, ERK1/2, and I

59 ciferase were also inhibited by MEKK1 siRNA, PD98059 (an MEK inhibitor), U0126 (an ERK inhibitor), an

60 B202190, but not 2'-amino-3'-methoxyflavone (PD98059), an inhibitor of p44/p42 MAPK activation, aboli

61 An anti-TGFbeta2 antibody and PD98059, an ERK activation inhibitor, inhibited SH-SY5Y

62 However, PD98059, an ERK inhibitor, had no effect.

63 orylation was prevented by pretreatment with PD98059, an ERK pathway inhibitor.

64 H222P) mice that develop cardiomyopathy with PD98059, an inhibitor of ERK activation.

65 PD98059, an inhibitor of mitogen-activated protein kinas

66 etreatment of porcine anterior segments with PD98059, an inhibitor of p42/44 MAP kinase pathway.

67 PD98059, an inhibitor of p44/42 MAPK kinase, blocked thr

68 In agreement, PD98059, an inhibitor of the ERK-activating enzyme MEK,

69 s rescued by intravitreous administration of PD98059, an inhibitor of the ERK1/2-activating kinase ME

70 t of JWH015 was blocked by pretreatment with PD98059, an inhibitor of the p42/44 MAP kinase pathway.

71 PD98059, an inhibitor of the p42/44 MAPK pathway, blocke

72 PD98059, an MEK1/2 inhibitor, also suppressed ERK1/2 act

73 ctivated protein kinase (MAPK)/ERK inhibitor PD98059 and antioxidant N-acetyl-l-cysteine restored nor

74 PD98059 and EP2 receptor blockade with AH6809 (6-isoprop

75 en-activated protein kinase kinase inhibitor PD98059 and Ets-1 silencing each abolished PGE(2)-induce

76 PD98059 and Ets-1 silencing each abrogated the effect of

77 ssociated protein-43, which was inhibited by PD98059 and GF109203X, indicating the involvement of mit

78 n of the corresponding upstream kinases with PD98059 and LY294002, respectively.

79 so seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apopto

80 ERK1/2 phosphorylation by the MEK inhibitors PD98059 and PD184161.

81 addition of the MAP/ERK1/2 kinase inhibitors PD98059 and PD184352.

82 y 2-fold) and could be inhibited by H-89 and PD98059 and potentiated by IBMX and cholera toxin (250 m

83 by human macrophages, which are inhibited by PD98059 and rapamycin (mTOR inhibitor).

84 In turn, MEK inhibitors U0126 and PD98059 and siRNA-mediated depletion of either ERK1 or E

85 bolished by the MAPK/ERK1/2 kinase inhibitor PD98059 and the epidermal growth factor (EGF) receptor i

86 Two of these inhibitors, PD98059 and TPCK, had anti-tumor activity as single agen

87 gonized by the p42,44 MAPK kinase inhibitors PD98059 and U0125.

88 inhibitors of the ERK1/2 signaling pathway, PD98059 and U0126 and the spleen tyrosine kinase (Syk) i

89 le inhibition of basal MEK-ERK activity with PD98059 and U0126 had little effect.

90 osing MEFs to the MEK1/2-specific inhibitors PD98059 and U0126 protected both KSR+/+ and KSR-/- MEFs

91 Inhibition of MEK1/2 activity using PD98059 and U0126 reduced Fra-1 expression, DNA binding,

92 activity, while the MEK-specific inhibitors PD98059 and U0126 reduced protein production of these cy

93 -Ras inhibitor FTI-277 and MEK1/2 inhibitors PD98059 and U0126 strongly inhibited JSRV transformation

94 of PI3K (LY294002 and wortmannin) and MAPK (PD98059 and U0126) on regional sympathetic responses to

95 ated by the MAPK/ERK kinase (MEK) inhibitors PD98059 and U0126, as well as by ADAM10 and -17 inhibito

96 Specific MEK1/2 inhibitors, flavenoid PD98059 and U0126, decreased the basal and TGF-beta1-sti

97 d VDR protein increase, while treatment with PD98059 and U0126, specifically blocked ERK phosphorylat

98 as dramatically attenuated by ERK inhibitors PD98059 and U0126.

99 oximately 15-30 min and that MEK1 inhibitors PD98059 and U0216 inhibit Smad3 phosphorylation induced

100 This effect is blocked almost entirely by PD98059 and UO126, implying involvement of the MEK/ERK s

101 permeability, and the effect was blocked by PD98059 and UO126, selective inhibitors of the mitogen-a

102 In addition, the MEK/ERK inhibitors, PD98059 and UO126, suppressed PMA-stimulated TRAF1 promo

103 ced CREB phosphorylation was reduced by both PD98059 and wortmannin.

104 amino-3-methoxyphenyl-4H-1-benzopyran-4-one (PD98059) and by PKA, PKC, and CaMK inhibitors.

105 Selective inhibitors of MAPK (PD98059) and PI-3 kinase (LY294002) suppressed HGF-induc

106 he MEK inhibitor 2'-amino-3'-methoxyflavone (PD98059) and the p38 inhibitor 4-(4-fluorophenyl)-2-(4-m

107 PI3K) inhibitors 2'-amino-3'-methoxyflavone (PD98059) and wortmannin reduced the neuroprotective effe

108 GE receptor, an ERK1/2 MAP kinase inhibitor (PD98059), and DN-MEK1, but not by a neutralizing TGF-bet

109 Inhibitors of PKA (KT5720), MAPK (U0126 and PD98059), and tyrosine kinase (genistein) blocked the lo

110 S since the specific inhibitors, wortmannin, PD98059, and dominant negative IKKbeta transgene express

111 ase DNA methyltransferase expression (U0126, PD98059, and hydralazine).

112 rase activity were inhibited by MEKK1 siRNA, PD98059, and RSK1 siRNA.

113 cts were of a magnitude similar to SP600125, PD98059, and SB202190, specific inhibitors of the JNK1/2

114 The specific Mek inhibitor PD98059 antagonized the okadaic acid-induced activation

115 ptor TrkB inhibitor ANA-12 and MEK inhibitor PD98059 attenuates the neurotrophic action of compounds.

116 diated macrophage survival was eliminated by PD98059, BI-D1870, or sc68376, the specific inhibitors f

117 inhibitor (NSC 87877), or the MEK inhibitor PD98059 blocked FSH-dependent ERK(Thr(202)/Tyr(204)) pho

118 Importantly, MEK 1 inhibitor PD98059 blocked only the hyperphosphorylation of Raf-1 b

119 Treatment of cells with PD98059 blocked phosphorylation of m- and mu-calpain and

120 The MAPK/ERK kinase inhibitor PD98059 blocked tamoxifen-resistant growth.

121 n target of rapamycin, and the MEK inhibitor PD98059 blocked the EtOH-induced phosphorylation of eEF2

122 (iii) The endocytosis inhibitor PD98059 blocked the replication in J1-1 cells of a mutan

123 MEK1/2 inhibitor 2'-amino-3'-methoxyflavone (PD98059) blocked the induction of EGR-1 expression by PG

124 Treatment of cells with staurosporine or PD98059 blocks both Bcl2 and c-Myc phosphorylation and r

125 MAPK and ERK1/2 activation, and SB203580 and PD98059 blunted IL-17-mediated NF-kappaB and C/EBP activ

126 ced phosphorylation of RSK2 was inhibited by PD98059 but not by wortmannin.

127 ively active MEK1 diminished the capacity of PD98059 but not PD184352 to block UCN-01-mediated Bim(EL

128 The restored dilation was insensitive to PD98059 but was blocked by TEA.

129 en-activated protein/ERK kinase 1 signaling (PD98059) but abrogated when cells were treated with the

130 inhibitor (wortmannin) and an ERK inhibitor (PD98059) but not by a p38-MAPK inhibitor (SB203580).

131 lar signal-regulated kinase (ERK) inhibitor (PD98059), but not an estrogen receptor blocker (ICI 1827

132 ted by the MEK-specific inhibitors U0126 and PD98059, but not by the PI3K-specific inhibitor wortmann

133 Treatment of U87MG.EGFRvIII cells with PD98059, but not LY294002, also resulted in increased ce

134 ith this, we observed that the MEK inhibitor PD98059, but not the phosphatidylinositol 3'-kinase inhi

135 whereas inhibition of Src by PP2 or MEK1 by PD98059 caused decreases in c-fos, fra-1 and c-jun expre

136 The inhibitors U0126, MIIC and PD98059 caused NAD(H) reduction, heme oxidation, and dec

137 Neither ERK1/2 inhibitor PD98059 alone nor PD98059 combined with LY37 treatment induced changes in

138 no effect on this aspect of insulin action, PD98059 completely blocked each of these responses.

139 Unexpectedly, the MEK inhibitor PD98059 completely blocks insulin-stimulated increase in

140 ted kinase (ERK) kinase (MEK)/ERK inhibitor, PD98059, completely abrogated the effect of high glucose

141 ivated ERK-activating kinase (MEK) inhibitor PD98059 converts their flat, process-bearing morphology

142 PD98059 cotreatment significantly inhibited SDF-1alpha-i

143 infusions of U0126 or another MEK inhibitor, PD98059, CPP retrieval and concomitant protein activatio

144 other hand, inhibitors of GSK3beta, but not PD98059 decreased ERK/pGSK3beta(Tyr-216) association and

145 ardiography demonstrated that treatment with PD98059 delayed the development of left ventricular dila

146 ng of the MAPK pathway by the MAPK inhibitor PD98059 did not affect normal development of rods in ret

147 n, whereas treatment with the MAPK inhibitor PD98059 did not block EGFR activation, indicating that E

148 PP2, and reported downstream ERK with 25 muM PD98059 did not prevent estrogen action but caused an in

149 (H89) and mitogen-activated protein kinase (PD98059) did not block the effect of serum on lipolysis,

150 02190) and ERK1/2 activation in LNCaP cells (PD98059) did not protect against guggulsterone-induced c

151 n of the p42/p44 MAPK kinase (MEK) inhibitor PD98059 during reperfusion abolishes the cardioprotectiv

152 Neither DFMO nor PD98059, either alone or in combination, reduced cdk-4 a

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

154 ell survival in hyperoxia, as treatment with PD98059 enhanced hyperoxia-mediated cell death.

155 Interestingly, PD98059 enhanced nuclear proapototic function of p53 in

156 The specific ERK1/2 inhibitor PD98059 enhanced the resolution of inflammation, whereas

157 reased by pretreatment of muscle fibers with PD98059 (ERK1/2 inhibitor) and removal of Ca2+ ions from

158 preincubated with specific MAPK inhibitors (PD98059 for MAP/ERK, SP600125 for JNK, and SB203580 for

159 e mitogen-activated protein kinase inhibitor PD98059 for postoperative days 1-4 reduced and nearly ab

160 e (LY294002) and 2'-amino-3'-methoxyflavone (PD98059) for both normal and HER2-overexpressing cells.

161 gainst p75(NTR) and the MAP kinase inhibitor PD98059 had no impact.

162 iene (U0126) and 2'-amino-3'-methoxyflavone (PD98059), had similar off-target effects.

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

164 of BRAF or treatment with the MEK inhibitor PD98059 impaired the translation of only HIF-2alpha.

165 pathway inhibitors (SB203580, curcumin, and PD98059) implicated p38 and JNK, but not ERK, in 8-iso-P

166 Inhibition of ERK activation by PD98059 in endothelial cells was shown to potentiate thr

167 ROSE cells with the MEK inhibitors U0126 and PD98059 increased Par-4 protein expression.

168 Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(

169 ed apoptosis, effects that were abolished by PD98059, indicating that inhibition of ERK plays a major

170 Moreover, MEK inhibition by PD98059 induces a significant increase of CRE-mediated g

171 MEK inhibitors UO126 and PD98059 inhibited both CagA-independent and -dependent M

172 mic treatment of Lmna(H222P/H222P) mice with PD98059 inhibited ERK phosphorylation and blocked the ac

173 PD98059 inhibited MEK1 whereas TPCK suppressed S6K1 acti

174 rk (DN-Erk) or pre-exposure to ERK inhibitor PD98059 inhibited NF-kappaB.

175 (1)R-mediated death, since the MEK inhibitor PD98059 inhibited Substance P-induced death in primary s

176 d3 small interfering RNA, or the addition of PD98059 inhibited TGF-beta1-dependent stimulation of TGF

177 t on ERK as treatment with the MEK inhibitor PD98059 inhibited the insulin effect (62% reduction, p =

178 Interestingly, LY294002, but not PD98059, inhibited wild-type EGFR pTyr in response to EG

179 PD98059 inhibition of MAPK was associated with a concent

180 omes and then infused with the MEK inhibitor PD98059 into the PL immediately after training failed to

181 gen-activated extracellular kinase inhibitor PD98059 is required to diminish proliferation in these c

182 -signal inhibitor; the MAPK signal inhibitor PD98059; lapatinib, which inhibits both the epidermal gr

183 ed protein kinase kinase-specific inhibitor, PD98059, led to regained surface CD40 expression and int

184 In the absence of PD98059, levels of fetal hemoglobin averaged 27.4% +/- 7

185 The addition of PD98059, LY294002, NAC, curcumin, EGCG, and SB203580 mar

186 on, TGM-2 induced by CsA is downregulated by PD98059, LY294002, NAC, curcumin, EGCG, and SB203580.

187 rved within 30 minutes, which was blocked by PD98059 [MAPK kinase (MEK) inhibitor].

188 vated protein kinase (MAPK) kinase inhibitor PD98059 markedly reduces induction of HIF-1 alpha by LMP

189 ot ICI182780 (estrogen receptor blocker), or PD98059 (MEK (MAPK/extracellular signal-regulated kinase

190 PD98059 (MEK-specific inhibitor) could reverse EGF-media

191 (protein kinase A inhibitor, 10 micromol/L), PD98059 (MEK1 inhibitor, 0.1 micromol/L), and wortmannin

192 lated ERK activation, and the ERK inhibitor, PD98059, mimicked PGE2 in blocking p65, but enhancing p5

193 Addition of the ERK inhibitor PD98059 mitigates these effects.

194 nd AKT is inhibited, respectively, by U0126, PD98059 (mitogen-activated protein kinase kinase inhibit

195 production (2.3-fold), which was blocked by PD98059, NAC, and DPI.

196 Administration of the PD98059-nanoparticles in melanoma-bearing mice inhibits

197 sed by treating the cells with an inhibitor (PD98059) of mitogen-activated protein kinase kinase (MEK

198 ecific inhibitor 2'-amino-3'-methoxyflavone (PD98059) of mitogen-activated protein kinase kinase, the

199 e examined the effects of the MEK1 inhibitor PD98059 on renal organ cultures and confirmed a previous

200 MAPK pathway with either the MEK1 inhibitor PD98059 or a dominant-negative Ras mutant, RasN17, aboli

201 PD98059 or another MEK inhibitor, 1,4-diamino-2,3-dicyan

202 lation in wild-type MEF by the MEK inhibitor PD98059 or by transient depletion of ERK1/2 via small in

203 PD98059 or calphostin C did not.

204 r fluids; induction of VEGF is suppressed by PD98059 or catalase.

205 However, in the presence of PD98059 or depletion of ERK1/2, exogenous Pref-1 cannot

206 nhibition of PtdCho synthesis was blocked by PD98059 or dominant-negative ERK (p42 kinase).

207 ERK1/2 inhibition with PD98059 or p38 with SB203580 blocked the effect of LXA4

208 kinase pathways with the chemical inhibitors PD98059 or SB203580 suggested that activation of these s

209 ence of either ERK1/2 or p38 MAPK inhibitor (PD98059 or SB203580) resulted in an additive inhibition

210 nt with the MEK1/2-ERK1/2 pathway inhibitors PD98059 or SL327, prior to each priming dose of SKF-3839

211 s not altered significantly by ERK inhibitor PD98059 or the JNK inhibitor SP600125.

212 nase (ERK)-activating kinase (MEK) inhibitor PD98059 or the Src kinase inhibitor PP2.

213 Inhibition of the MAPK pathway with PD98059 or U0126 blocked the DFMO-induced induction of p

214 activation in HepG2 human hepatoma cells by PD98059 or U0126 blocked the increased phosphorylation o

215 MDA-MB-435 cells treated with PD98059 or U0126 in the presence and absence of DFMO exh

216 3-9006 but not the MAP/ERK kinase inhibitors PD98059 or U0126 induced the nuclear translocation of ap

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

218 tion was blocked by MEK-specific inhibitors (PD98059 or U0126).

219 of Smad2/3 (SB431542 or LY364947) or ERK1/2 (PD98059 or U0126)].

220 y pharmacological inhibition of ERK1/2 using PD98059 or U0126.

221 t of tumour cells with the MEK1/2 inhibitors PD98059 or U0216, or expression of a dominant-negative f

222 on of the MAPK/ERK kinase 1 (MEK1) inhibitor PD98059 or use of Tg mice in which a dominant-negative M

223 r Akt phosphorylation is blocked upstream by PD98059 or Wortmannin or LY294002, respectively.

224 lowing treatment with TGFbeta1, ethanol, and PD98059 (or U0126) plus ethanol.

225 APK) activation, 2'-amino-3'-methoxyflavone (PD98059) or 1,4-diamino-2,3-dicyano-1,4-bis(2-aminopheny

226 n was blocked by 2'-amino-3'-methoxyflavone (PD98059) or 1,4-diamino-2,3-dicyano-1,4-bis(methylthio)b

227 e also pretreated with an MEK-1/2 inhibitor (PD98059) or a p38 inhibitor (SB203580) and an anti-CTGF

228 gnaling, either by the use of MEK inhibitor (PD98059) or by siRNA specific to B-Raf, significantly lo

229 activation with SN50 or ERK1/2 activation by PD98059, or by inhibition of phosphoinositide-3 kinase (

230 -l-methionine, the specific ERK1/2 inhibitor PD98059, or infection of a recombinant adenovirus encodi

231 alpha-cyanocinnamate (CDC), ERK1/2 inhibitor PD98059, or p38 inhibitor SB203580.

232 th the MEK inhibitor U0126, ERK1/2 inhibitor PD98059, or small interference RNA targeted to ERK1/2 at

233 s using pharmacological inhibitors ZK159222, PD98059, or SP600125, respectively, inhibited pRb and C/

234 bitor PKA inhibitor (PKI), the MEK inhibitor PD98059, or the ribosomal S6 kinase-2 (RSK-2) inhibitor

235 inase inhibitor LY294002, the MAPK inhibitor PD98059, or the translational inhibitor cycloheximide.

236 Inhibition of p44/42 ERKs (PD98059), p38 MAPK (SB203580), Akt, and PI3K (LY294002),

237 Specific inhibitors for ERK1/2 MAPK (PD98059), p38 MAPK (SB203580), JNK MAPK (SP600125), or P

238 racellular signal-regulated kinase inhibitor PD98059 partially reduced EGF effects.

239 ular signal-regulated kinase (ERK) inhibitor PD98059, phosphatidylinositol 3-kinase inhibitor LY29400

240 tor (staurosporine), MEK-specific inhibitor (PD98059), PI3 kinase inhibitor (LY294002), or PKA inhibi

241 rference, SiRNA, or FRNK transfection), MEK (PD98059), PKC (calphostin C), and actin destabilization

242 (CaMKKbeta) using the inhibitors wortmannin, PD98059, PP2, and STO-609, respectively.

243 Indeed, PD98059 prevented Nanog repression induced by ES cell ag

244 PD98059 prevented p53-mediated induction of p21 at the t

245 nscription factor AP-1 by TGF-beta1, whereas PD98059 prevented TGF-beta1-dependent nuclear factor-kap

246 mino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) prevented the quinpirole-evoked increase in ASP

247 ation of ERK in monocytes and ERK inhibitor, PD98059, prevented the chronic alcohol-induced increase

248 f these cells with the MAPK kinase inhibitor PD98059 prior to infection blocked the increase in phosp

249 bitors for GSK3beta (TDZD and LiCl) and ERK (PD98059) protected cells from FGF2-induced apoptosis.

250 e mitogen-activated protein kinase kinase by PD98059 reduced the level of HIF-1alpha only in normoxic

251 Although the MAPKK inhibitor PD98059 reduced the number of surviving neurons in S100B

252 RK phosphorylation using the MEK-1 inhibitor PD98059 rescued approximately 30% of cells from bFGF-ind

253 nhibition with 10 microM SB203580 and 10 muM PD98059, respectively.

254 by treatment of cells with the ERK inhibitor PD98059 resulted in the increase in CIITA-mediated gene

255 tivation via the MEK1/2 inhibitors U0126 and PD98059 results in decreased Stx1-mediated IL-8 mRNA.

256 ion of the ERK pathway, as the ERK inhibitor PD98059 reversed ox-PAPC inhibitory effects on BMP-2-ind

257 PD98059 reversed the G2-M block induced by DFMO (probabl

258 The MEK1/2 inhibitors U0126 and PD98059 reversed the protective effects of COL1 and the

259 Conversely, inhibition of ERK activity by PD98059 reversed the R115777-induced inhibition of STAT3

260 protein kinase kinase inhibitors, U0126 and PD98059, reversed BNP inhibition of TGF-beta-induced col

261 phorylation, an effect that was inhibited by PD98059, rottlerin, and protein kinase Cepsilon (PKCepsi

262 Inhibition of ERK activation by U0126 or PD98059 significantly decreased EGF-dependent COX-2 expr

263 Specifically, PD98059 significantly decreased the total number of macr

264 st, specifically blocking MAPK activity with PD98059 significantly increased BEC TFF3 expression.

265 protein kinase (MAPK) signaling by U0126 and PD98059 significantly reduced the UVR response whereas o

266 racellular signal-regulated kinase inhibitor PD98059, significantly decreased high-glucose-induced IL

267 ide, but not wortmanin or the MAPK inhibitor PD98059, significantly decreased production of RANTES, i

268 mitogen-activated protein kinase inhibitor), PD98059 (specific MEK inhibitor), SP600125 (JNK inhibito

269 with alpha2M*, 2) the MAP kinase inhibitor, PD98059, specifically blocked the alpha2M*-induced neuri

270 1 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a,

271 We also found that PD98059 strongly attenuated progression of HeLa cells th

272 ffects being abrogated by the MEK inhibitor, PD98059, suggesting a role for ERK signaling in alpha2-m

273 pamycin inhibitor, but not by MAPK inhibitor PD98059, suggesting that insulin exerts its effect on SN

274 n of GADD34 did not block the sensitivity to PD98059, suggesting that MEK functions to enhance GCN2-d

275 togen-activated protein kinase kinase (MEK) (PD98059), the cSrc-family tyrosine kinase (PP1), or the

276 However, PD98059, the ERK1/2 cascade pathway inhibitor, was ineff

277 nal-regulated kinase (ERK) pathway inhibitor PD98059, the nonselective potassium channel blocker tetr

278 ion were examined using the ERK1/2 inhibitor PD98059, the Src inhibitor pp2, the nuclear factor- kapp

279 bitors were reduced in cells pretreated with PD98059 to inhibit ERK.

280 4002 to inhibit the PI 3-kinase pathway, and PD98059 to inhibit the MAP kinase-dependent pathway.

281 microM SB203580/SB202190) or ERK (50 microM PD98059) to delineate the role of p38 and ERK in IL-12-m

282 PD98059-treated Lmna(H222P/H222P) mice had normal cardia

283 30 micromol/L (n=5) and 50 micromol/L (n=5) PD98059 treatment (-11.0+/-0.8% and -14.6+/-2.0%, respec

284 multipathway model in analogously predicting PD98059 treatment effects on cell migration.

285 vation of transcription-dependent apoptosis, PD98059 treatment promoted the translocation of p53 from

286 As predicted, PD98059 treatment reduced cdk-2 activity and Rb phosphor

287 bserved sensitivity of AMPK to rapamycin and PD98059 treatments.

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

289 pathway using the pharmacological inhibitors PD98059, U0126, and SB203580 in T98G LGI1-null cells inh

290 nzo-p-dioxin (TCDD) and Erk kinase inhibitor PD98059, U0126, or SL327 led to enhanced nuclear accumul

291 d biochemical and pharmacological inhibitor (PD98059, U0126, SB203580, SP600125) approaches positione

292 Inhibition of EGFRvIII pTyr by PD98059 was not observed to be phosphorylation site spec

293 rough inhibition studies using genistein and PD98059 we found that the Pyk-2 tyrosine kinase-ERK1/2 p

294 en-activated protein kinase kinase inhibitor PD98059, we found that Nef-induced Erk signaling is esse

295 kinase inhibitor LY294002 and MAPK inhibitor PD98059 were found to significantly reduce leptin-induce

296 mitogen activated protein kinase antagonist PD98059 were unable to antagonize the immediate neuropro

297 LY294002 and PD98059 were used to define the role of specific ras eff

298 he phosphorylation at Ser-112 was blocked by PD98059, whereas the phosphorylation at Ser-136 was bloc

299 MEK1/2 kinase inhibitors, such as U0126 and PD98059, which inhibit the ERK1/2 activation and subsequ

300 We found that PD98059, which itself has minimal apoptogenic activity,