ライフサイエンスコーパス: PD098059

1 ed protein kinase kinase 1 or 2 (MKK1/2 with PD098059).

2 -7 cells were treated with the MEK inhibitor PD098059.

3 n, and this increase was further enhanced by PD098059.

4 cells treated with rapamycin, wortmannin, or PD098059.

5 l-related kinase-activating enzyme inhibitor PD098059.

6 control DMSO or the MAP/Erk kinase inhibitor PD098059.

7 er by cAMP or directly by the MAPK inhibitor PD098059.

8 ty and apoptosis induced by vinblastine plus PD098059.

9 s also totally prevented by PP2, AG1478, and PD098059.

10 n OK cells pretreated with the MEK inhibitor PD098059.

11 llular signal-regulated kinase is blocked by PD098059.

12 ular signal-regulated kinase (MEK) inhibitor PD098059.

13 completely, inhibited by the MEK1 inhibitor PD098059.

14 inhibition of p42(mapk/erk2) activation with PD098059.

15 MAPK since these responses were inhibited by PD098059.

16 nuclear translocation was also eliminated by PD098059.

17 nduced ERK phosphorylation was eliminated by PD098059.

18 ion was attenuated by the specific inhibitor PD098059.

19 der hypoxic conditions was also inhibited by PD098059.

20 nt MEK1S218/222A and the MEK1/MEK2 inhibitor PD098059.

21 in and mitogen-activated protein kinase with PD098059.

22 nding cell lines are not growth inhibited by PD098059.

23 bited by pretreatment with the MEK inhibitor PD098059.

24 onditioning was blocked by pretreatment with PD098059.

25 or the synthetic MAP kinase kinase inhibitor PD098059.

26 was reversed by the simultaneous addition of PD098059.

27 finity for deltaN3-S218E/S222D MEK than does PD098059.

28 r in cells pretreated with the MEK inhibitor PD098059.

29 tracellular-response kinase kinase inhibitor PD098059 (10(-5) M) inhibited the IGF-1 effect.

30 The addition of PD098059 (40 microM; EC50 = 10 microM) during a 30-min w

31 phosphorylation level was inhibited by KN93, PD098059 (a MAPK kinase (MEK) inhibitor) and calcium dep

32 ed stronger inhibitory effects compared with PD098059 (a well known pharmacological inhibitor of MEK)

33 ditioning was inhibited by pretreatment with PD098059, A MEK1 (ERK-Activating kinase) inhibitor.

34 atment of hypertonically stressed cells with PD098059, a mitogen-activated extracellular regulated ki

35 Here, we report that PD098059, a selective inhibitor of the calcium-activated

36 PD098059, a specific inhibitor of MEK-1, prevented the d

37 PD098059, a specific inhibitor of mitogen-activated prot

38 ncogenes and growth factors was inhibited by PD098059, a specific MAP kinase kinase (MEK) inhibitor.

39 tivation for megakaryocytic differentiation, PD098059, a synthetic inhibitor of the MAP kinase kinase

40 tin exerted stronger inhibitory effects than PD098059, a well-known pharmacologic inhibitor of MEK.

41 PD098059 also inhibited the stimulation of Akt phosphory

42 PD098059 also interfered with NK lysis of tumor cells in

43 etreatment with suramin or the MEK inhibitor PD098059 also potentiated the toxicity of BHTOOH.

44 PD098059, an ERK pathway inhibitor, does not affect HO-1

45 PD098059, an ERK1/2 inhibitor, opposed ERK1/2 activation

46 independent growth is strongly inhibited by PD098059, an inhibitor of Mek/ MAP kinase kinase.

47 We found that PD098059, an inhibitor of mitogen-activated protein (MAP

48 iminated when the cells were pretreated with PD098059, an inhibitor of mitogen-activated protein kina

49 dent manner, and the effect was inhibited by PD098059, an inhibitor of the ERK1/2 signaling pathway.

50 by using MAP kinase kinase (MEK1) inhibitor PD098059 and a dominant negative Erk2, as well as wild-t

51 l migration was blocked by the MEK inhibitor PD098059 and by dominant negative MEK-1, indicating an e

52 ctivated protein kinase/ERK kinase inhibitor PD098059 and dominant-negative Ras and Raf mutants but n

53 Both PD098059 and SB203580 inhibited FMLP-stimulated superoxi

54 pathway, we used the specific MEK1 inhibitor PD098059 and the PI3'K inhibitor LY 294002.

55 vated protein kinase kinase (MEK) inhibitors PD098059 and U0126 showed that integrin alpha2 expressio

56 wo structurally unrelated inhibitors of MEK (PD098059 and U0126), we provide evidence that Erk activa

57 , a selective inhibitor of the p38 MAPK, and PD098059 and UO126, both selective inhibitors of the ERK

58 of the specific MAP kinase kinase inhibitor, PD098059, and wortmannin, a PI 3-kinase inhibitor, sugge

59 Interestingly, both PD098059- and UO126-infused animals also demonstrated an

60 did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK ac

61 hibitor PD098059 demonstrates that U0126 and PD098059 are noncompetitive inhibitors with respect to b

62 nd the increase was significantly blocked by PD098059 as well as by both KN93 and antisense oligodeox

63 Introduction of PD098059 at any time during the first 18 h of TPA treatm

64 The MEK inhibitor PD098059 attenuated GH-induced expression of the endogen

65 ng activities of Nrf2, and SB203580, but not PD098059, attenuates Nrf2-mediated trans-activation of p

66 led to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did

67 ely active mutant of MEK2 could override the PD098059 blockade.

68 Moreover, inhibition of MEK with PD098059 blocked FGF-2-induced proliferation in H-510 ce

69 The MEK inhibitor, PD098059, blocked the growth-promoting activity of uPA a

70 cked not only by the MEK-specific antagonist PD098059, but also by antagonists of the Rho-Rho kinase

71 Notably, MAPK inactivation with PD098059, but not Ras inactivation with FTI-277, could i

72 Surprisingly, PD098059 caused a dramatic enhancement of differentiatio

73 PD098059 completely neutralized the effects of uPA on MC

74 A specific MAPK pathway inhibitor, PD098059, could block not only MAPK activation but also

75 Furthermore, the MEK inhibitor, PD098059, decreased the motility of RAP-treated cells wi

76 etic analysis of U0126 and the MEK inhibitor PD098059 demonstrates that U0126 and PD098059 are noncom

77 PD098059 did not alter the IGF-I suppressive effect on s

78 s to rapidly activate MAPK within 5 min, and PD098059 effectively blocked both MAPK activation and tu

79 After 24 h of TPA treatment, introduction of PD098059 failed to block differentiation.

80 Inhibiting ERK1/2 (30 mumol/L PD098059 for 30 minutes) or chelating intracellular Ca2+

81 RK activation since the ERK kinase inhibitor PD098059 had no effect on IL-8-induced cell migration of

82 On the other hand, the MEK kinase inhibitor PD098059 had no effects, further demonstrating the speci

83 In contrast, the Mek inhibitor PD098059 has no effect on survival.

84 MAPK with the specific MAPK kinase inhibitor PD098059 impairs the ability of HGF to promote cell surv

85 ng by the MAPK/ERK kinase (MEK)1/2 inhibitor PD098059 in combination with vinblastine robustly induce

86 and JunB is inhibited by the MEK1 inhibitor PD098059, indicating that the Raf-MEK-MAPK cascade is re

87 is pathway by the MEK inhibitors CI-1040 and PD098059 induced apoptosis through a unique pathway invo

88 PD098059 inhibited activation of p44/p42 MAPK in cholang

89 en-activated protein kinase kinase inhibitor PD098059 inhibited Ang II-induced MCP-1 gene expression,

90 mulation by the MAP kinase cascade inhibitor PD098059 inhibited epinephrine-promoted AA release.

91 PD098059 inhibited lipolysis by 53% in mice as well.

92 The MAPK kinase (MEK) inhibitor PD098059 inhibited phagocytosis, MLCK activity, and ERK2

93 PD098059 inhibited UVB- or UVC-induced AP-1 activity and

94 n of protein synthesis and eIF4F assembly by PD098059 is not through inhibition of eIF4E phosphorylat

95 A MEK-specific inhibitor (PD098059) is capable of blocking the activation of MAP k

96 en-activated protein kinase kinase inhibitor PD098059 markedly reduced induction of HIF-1 by mersalyl

97 ed protein kinase/ERK kinase (MEK) inhibitor PD098059 minimally inhibited PE-induced increases in CSA

98 By contrast, neither an ERK inhibitor (PD098059) nor p38 inhibitors (SB203580 and SB202190) had

99 Differentiation blockade by PD098059 occurred via inhibition of MEK because transfec

100 roprotection could be caused by an effect of PD098059 on seizure-like events or on downstream signali

101 l injection of the MAPK/ERK kinase inhibitor PD098059 or after a continuous 7 d intrastriatal infusio

102 ivation, either by the pharmacologic reagent PD098059 or by dominant-negative MAPK kinase (MEK) expre

103 cortactin in the presence of either H(2)O(2)/PD098059 or H(2)O(2) alone at 200 microm exhibited a dra

104 ifferentially inhibited by the MEK inhibitor PD098059 or the p38 MAP kinase inhibitor SB202190.

105 MAPK kinase 1 (MEK1) inhibitor PD098059 or the protein tyrosine kinase inhibitor genist

106 73122), and is abolished by a MEK inhibitor (PD098059) or dominant negative Ras.

107 uced by 25 micromol/L of the MEK1 inhibitor (PD098059) or the PI 3-kinase inhibitor (LY294002).

108 imately 50%) inhibited by the MEK inhibitor, PD098059, or by co-transfection of kinase-inactive MEK1

109 MEK-1 inhibitor PD098059 partially blocked MMP-9 activation, whereas PI3

110 Moreover, PD098059 prevented the HGF/SF-induced migration of Rama

111 ctivated protein kinase/ERK kinase inhibitor PD098059 reduced ERK activation by 90%, while an inhibit

112 r, tyrphostin AG1478, and the MEK inhibitor, PD098059, restores the normal level of Lot1 gene express

113 rmacologic inhibitors of MAPKs, SB203580 and PD098059, revealed that priming of the respiratory burst

114 PD098059 significantly attenuated PTH inhibition of phos

115 dehydroxymethylepoxyquinomicin, bortezomib, PD098059) that target survival/antiapoptotic pathways.

116 in addition to the MAP/Erk kinase inhibitor PD098059, the PI 3-kinase inhibitors LY294002 and wortma

117 cells with the MAP kinase cascade inhibitor PD098059, the PKC inhibitor GF109203X, or down-regulatio

118 intra-EC infusion of ERK cascade inhibitors (PD098059, UO126) at 40 min, but not at 10 min, resulted

119 Using the selective MEK inhibitor PD098059, we were able to block the feedback desensitiza

120 When wortmannin and PD098059 were given together, the effect was synergistic

121 ream regulator of eIF4E phosphorylation, and PD098059, which is a MEK inhibitor that blocks Erk activ

122 and chromatin condensation are inhibited by PD098059, which selectively inhibits MAPK kinase, an ups