ライフサイエンスコーパス: GF109203X

1 ompletely prevented by PKC inhibition (1 mum GF109203X).

2 by the PKC inhibitor bisindolylmaleimide I (GF109203X).

3 ,13-dibutyrate) but not by pretreatment with GF109203X.

4 25(FAK) phosphorylation either alone or with GF109203X.

5 onfirmed by using the PKC-specific inhibitor GF109203X.

6 reversed by treatment with the PKC inhibitor GF109203X.

7 calmidazolium but not by pertussis toxin or GF109203X.

8 were abolished by pretreatment of cells with GF109203X.

9 d to respond to phorbol myristate acetate or GF109203X.

10 by candesartan and a general PKC inhibitor, GF109203X.

11 U71322 and protein kinase C (PKC) antagonist GF109203X.

12 er mimicked nor blocked by the PKC inhibitor GF109203X.

13 r necrosis factor-alpha was not inhibited by GF109203X.

14 is much slower in Jurkat cells treated with GF109203X.

15 inase C (PKC) inhibitors H-7 (30 microM) and GF109203X (1 microM) or the PKC activator phorbol 12-myr

16 ked by the PKC inhibitors H-7 (30 microM) or GF109203X (1 microM).

17 The bisindolylmaleimide, GF109203X (2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3

18 er sensitive to the selective PKC inhibitors GF109203x (2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3

19 ed by an inhibitor of protein kinase C (PKC; GF109203X, 3 microM) or by omission of ATP from the pipe

20 1 microM), or the protein kinase C inhibitor GF109203X (5 microM) prevents platelet activation by mic

21 lls with a protein kinase C (PKC) inhibitor (GF109203X; 5 microM) abolished basal phosphorylation and

22 tagonist ZM241385, they were both blocked by GF109203X (a selective inhibitor of conventional and nov

23 in kinase D (PKD) and PKCalpha, but not with GF109203X, a general inhibitor of PKCs, suggesting PKD a

24 Nonetheless, neither GF109203X, a PKC inhibitor, nor BAPTA-AM, a calcium chel

25 bitors: PD98059, a MAP kinase inhibitor, and GF109203X, a protein kinase C (PKC) inhibitor.

26 In contrast, GF109203X, a selective inhibitor of classical PKC and PK

27 e p85 subunit of PI 3-kinase by 40%, whereas GF109203X, a specific inhibitor of PKC, partially preven

28 In contrast, the PKC inhibitor GF109203X abolished phenylephrine- and A61603-induced in

29 GF109203X abolished the inhibitory effects of halothane,

30 phorbol esters nor the inhibition of PKC by GF109203X affected the ability of Ro-31-8220 to activate

31 PLC inhibitor U73122, and the PKC inhibitor GF109203X all inhibited activation of TRPC1 SOCs, and U7

32 Furthermore, GF109203X alone caused a dose-dependent increase in glyc

33 ibitors calphostin C and bisindolylmaleimide GF109203X also abolished YT-mediated cytotoxicity.

34 GF109203X also blocked the inhibitory effect of PMA on c

35 ted activation of TRPC1 SOCs, and U73122 and GF109203X also reduced store-operated PKC-dependent phos

36 levels can be prevented by the PKC inhibitor GF109203X, an indication of the requirement for PKC kina

37 c PMA treatment and is severely inhibited by GF109203X, an inhibitor of PKCs.

38 GF109203X, an inhibitor of protein kinase C and the phos

39 Using GF109203X, an inhibitor of protein kinase C signaling, w

40 Selective inhibitors of PKC such as GF109203X and Calphostin C both caused approximately 80%

41 Two specific protein kinase C inhibitors, GF109203X and calphostin C, block TGFbeta-induced cluste

42 tion, while two selective inhibitors of PKC, GF109203X and chelerythrine chloride, effectively block

43 The PKC inhibitors GF109203x and Go6983 blocked BK activation by UTP in con

44 n of cells with selective inhibitors of PKC (GF109203X and Go6983) or c-Src (PP2).

45 While using GF109203X and Ro-31-8220 to address the role of PKC in i

46 itors are the structurally related compounds GF109203X and Ro-31-8220, both of which potently inhibit

47 y was inhibited by PKC selective inhibitors, GF109203X and Ro-32-0432.

48 tion of the protein kinase C (PKC) inhibitor GF109203X and the Ca(2+) calmodulin-dependent kinase II

49 otensin II plus PD123319 was blocked also by GF109203X and tyrphostin AG1478.

50 in kinase C inhibitors (bisindolylmaleimide (GF109203X) and calphostin C) blocked the activation of N

51 -1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide (GF109203X) and resulted from an effect at the level of t

52 pathway using inhibitors of PKA (THFA), PKC (GF109203X), and MAPK (UO126); and 4) mineralization eval

53 lpha(i) (pertussis toxin), protein kinase C (GF109203X), and phosphatidylinositol 3-kinase (wortmanni

54 on was inhibited by a general PKC inhibitor, GF109203X, and a mitogen-activated protein kinase kinase

55 directed toward the catalytic domain of PKC, GF109203X, and a selective inhibitor of PKC-delta, Rottl

56 Both a protein kinase C inhibitor, GF109203X, and a Src inhibitor, PP1, attenuated 5-HT-sti

57 s increase was inhibited by a PKC inhibitor, GF109203X, and antioxidants N-acetylcysteine (NAC) and r

58 affected by the protein kinase C inhibitor, GF109203X, and was only partially impaired by pretreatme

59 In parental MCF-7 cells, PKC inhibitors (GF109203X (bisindolylmaleimide I) and staurosporine) red

60 eatment of OCCM cells with the PKC inhibitor GF109203x (bisindolylmaleimide) significantly decreased

61 Inhibiting PKC activation with GF109203X blocked induction of c-fos by EGF but did not

62 The PKC inhibitor GF109203X blocked PMA- and bombesin- stimulated sst2A ph

63 A general PKC inhibitor, GF109203X, blocked the effect of Ang II on O(1.47 +/- .2

64 Calphostin C and GF109203X, both specific inhibitors of PKC, each inhibit

65 d by the specific protein kinase C inhibitor GF109203X, but not by PD98059, an inhibitor of MEK1/2 ki

66 nsensitive to the protein kinase C inhibitor GF109203X, but was blocked by the epidermal growth facto

67 -7) or specific protein kinase C inhibitors (GF109203x, calphostin C or chelerythrine) but not by tyr

68 in kinase C inhibitor Bisindolylmaleimide I (GF109203X) caused dramatic protection from loss of growt

69 T-7/mpl cells to the selective PKC inhibitor GF109203X completely inhibited the PKC activity associat

70 ion with the PKC inhibitors Calphostin C and GF109203X demonstrated that PKC is involved in PMA-regul

71 the nonselective protein kinase C inhibitor GF109203X did not interfere with SP-induced effects.

72 GF109203X displays none of these properties.

73 The protein kinase C (PKC) inhibitor GF109203X enhanced the glutamate-induced current, and th

74 ective inhibitors of protein kinase C (PKC), GF109203X (GF) and Ro318425 (Ro), significantly enhanced

75 administration of a selective PKC inhibitor GF109203X (GF, 0.73 nmol) in rats chronically implanted

76 phosphorylation using the pan-PKC inhibitor GF109203X (GFX).

77 In contrast, GF109203X had no effect on the TPO-induced expression of

78 n-regulation, the protein kinase C inhibitor GF109203X had no effect.

79 r PD98059 and the protein kinase C inhibitor GF109203X had no effect.

80 A PKC inhibitor (GF109203X) had no effect.

81 However, PKC inhibitor GF109203X has no effect on SP-dependent SPR phosphorylat

82 PIIIa expression was completely inhibited by GF109203X in a dose-dependent manner (IC50 = 0.5 mumol/L

83 PTP is sensitive to the PKC inhibitor GF109203X in both control and cKO.

84 Furthermore, the PKC-specific inhibitor, GF109203X, increased IGF-1-induced phospho-Ser-473-Akt a

85 he upregulation of neurectodermal markers to GF109203X indicates that the activity of a calcium activ

86 otein-43, which was inhibited by PD98059 and GF109203X, indicating the involvement of mitogen-activat

87 h the PKA inhibitor H89 or the PKC inhibitor GF109203X, individually or in combination reduced the ea

88 wever, were observed: at low concentrations, GF109203X inhibited AA release promoted by ATP, UTP, or

89 GF109203x inhibited phorbol ester-induced contraction of

90 The PKC inhibitor GF109203X inhibited PMA-induced, but not basal or EGF-in

91 , at higher concentrations (over 20 microM), GF109203X inhibited UVB-induced activation of JNKs, Erks

92 The PKC inhibitor bisindolylmaleimide 1 (GF109203X) inhibited MOR1 phosphorylation under basal co

93 the protein kinase C inhibitors, Go6983 and GF109203X, inhibited cholesterol accumulation.

94 etreatment with the selective PKC inhibitor, GF109203X, inhibited TPA-induced p125(FAK) tyrosine phos

95 PD98059 and GF109203X, inhibitors of ERK1/ERK2 pathway and PKC, resp

96 GF109203X is a stronger inhibitor of classical PKC than

97 Since GF109203X is more selective for PKCalpha, PKCalpha may a

98 Lower concentrations of GF109203X (<10 microM) had no effect on UVB-induced acti

99 Meanwhile, rottlerin and GF109203X markedly inhibited UVB-induced apoptosis of JB

100 NF-kappa B activation was blocked by either GF109203x, MG132, PDTC, or gliotoxin.

101 of hyperglycemia-induced PAI-1 expression by GF109203X, NAC, and GSH.

102 PKC inhibitor GF109203X nearly abolished PTP in both control and cKO.

103 Neither the PKC inhibitor GF109203X nor mutation of Ser-328, the site for PKC phos

104 Differential effects of GF109203X on cPLA2-mediated AA release and MAP kinase ac

105 In contrast to the inhibitory effect of GF109203X on GPIIIa expression, hemin induction of glyco

106 tors of MEK1 (PD98059) and protein kinase C (GF109203X) only partially inhibited duodenase-induced DN

107 protein kinase-C inhibitors (i.e., 4 microM GF109203X or 5 microM rottlerin).

108 In cells pretreated with 100 nmol/L GF109203X or 5 mumol/L chelerythrine (protein kinase C i

109 eatment with the preferential PKC inhibitors GF109203X or Go6983 profoundly inhibited PKD activation

110 The PKC inhibitors Go6976 and Gf109203x or nicardipine blocked increases in pT38 and p

111 a general protein kinase C (PKC) inhibitor, GF109203X or PKCbeta isoform inhibitor, LY333531 enhance

112 on of extensor digitorum longus muscles with GF109203X or rottlerin significantly attenuated increase

113 In contrast, PKC inhibitors GFX (GF109203X) or staurosporine prevented the activation of

114 of protein kinase C (PKC) with the inhibitor GF109203X, or by down-regulation of PKC, blocked the EGC

115 ascade inhibitor PD098059, the PKC inhibitor GF109203X, or down-regulation of PKC by PMA treatment, a

116 tor apigenin, the protein kinase C inhibitor GF109203X, or expression of a dominant negative form of

117 hibition of protein kinase C with Ro31-8220, GF109203x, or Go6976 or down-regulation of protein kinas

118 inhibited by the protein kinase C inhibitor, GF109203X, or thapsigargin, alone or in combination.

119 ntagonist of intracellular calcium release), GF109203X (PKC inhibitor), or PD98059 (MEK1/2 inhibitor)

120 t activated p38 kinase, and a PKC inhibitor, GF109203X, prevented its activation.

121 SB203580 nor the protein kinase C inhibitor GF109203X, protected insulin gene expression and secreti

122 cellular signal-regulated kinase inhibitor), GF109203X (protein kinase C inhibitor), and tyrphostin A

123 was observed with protein kinase C inhibitor GF109203X, rapamycin, or heparin.

124 GF109203X reduced TyrP of only the PYK2 sites, pY402 and

125 o-kinase (Y27632) and protein kinase C (PKC; GF109203X) reduced contraction and CPI-17 phosphorylatio

126 The PKC inhibitor, GF109203X, reduced the average mIPSC amplitude in neuron

127 or Src, but PKC depletion or incubation with GF109203X resulted in Ang II-dependent EGF receptor tyro

128 GF109203X, Ro 31-8220, calphostin C, and chelerythrine (

129 is diminished by pretreatment with either or GF109203x, suggesting involvement of multiple kinases.

130 eatment of cells with specific PKC inhibitor GF109203X, suggesting that the PKC pathway negatively re

131 Likewise, PKC inhibitor GF109203X suppressed ERK and p38 phosphorylation and PAR

132 632 and the protein kinase C (PKC) inhibitor GF109203X suppressed phosphorylation of MYPT1 Thr(850) a

133 A general PKC inhibitor, GF109203X, suppressed PDGF-BB's induction of ET-1 mRNA.

134 GF109203X, thapsigargin, or their combination partially

135 nhibited by protein kinase C (PKC) inhibitor GF109203X, the antioxidant N-acetylcysteine, and the red

136 xes is stimulated by PMA and is inhibited by GF109203X, thereby linking c-Raf-1 activation in this co

137 the presence of a protein kinase C inhibitor GF109203X, this impairment was not seen, indicating medi

138 More important, GF109203X treatment of Jurkat cells prior to T cell rece

139 hanges, Northern blot analysis revealed that GF109203X treatment reduced the steady-state level of GP

140 because it was blocked by chelerythrine and GF109203X, two PKC inhibitors.

141 This PMA stimulation was blocked by GF109203X, whereas basal internalization was unaffected.

142 arrest and was blocked by the PKC inhibitor GF109203X, which antagonized TPA-induced growth inhibiti

143 GF109203X with thapsigargin decreased TyrP of pY402PYK2