ライフサイエンスコーパス: bisindolylmaleimide

1 prevented by coaddition of the PKC inhibitor bisindolylmaleimide.

2 sensitive to the protein kinase C inhibitor, bisindolylmaleimide.

3 ed ATP or KN-62, and completely inhibited by bisindolylmaleimide.

4 rylation was inhibited with a PKC inhibitor, bisindolylmaleimide.

5 Pretreatment with bisindolylmaleimide (0.1 microM), a specific PKC inhibit

6 C-eta cells was blocked by the PKC inhibitor bisindolylmaleimide (0.5 micrometer) and the MEK inhibit

7 The PKC inhibitor bisindolylmaleimide 1 (GF109203X) inhibited MOR1 phospho

8 he Ca2+-dependent protein kinase C inhibitor bisindolylmaleimide 1, but was completely blocked by the

9 w approaches to the synthesis of macrocyclic bisindolylmaleimides 1-4 have been identified.

10 The protein kinase C (PKC) inhibitor bisindolylmaleimide (1 microM) completely blocked PMA/FP

11 ble receptors or the selective PKC inhibitor bisindolylmaleimide (1 microM).

12 Chelerythrine and bisindolylmaleimide-1 (Bis), two inhibitors of PKC, both

13 y either acute inhibition of PKC with 300 nm bisindolylmaleimide-1 (bis-1) or chronic down-regulation

14 Pan protein kinase C inhibitor bisindolylmaleimide-1 protected the cells from apoptosis

15 PDBu was antagonized by bisindolylmaleimide, a PKC inhibitor, and ruthenium red,

16 , whereas pretreatment of the platelets with bisindolylmaleimide, a protein kinase C inhibitor that p

17 I inhibitor, and only partially repressed by bisindolylmaleimide, a protein kinase C inhibitor.

18 by PDBu, and it persisted in the presence of bisindolylmaleimide, a selective PKC inhibitor.

19 that do not activate PKC and was blocked by bisindolylmaleimide, a specific PKC inhibitor.

20 Screening the conformationally diverse bisindolylmaleimides against a panel of protein kinases

21 ted >90% by the S6K inhibitors rapamycin and bisindolylmaleimide and by S6K1 silencing using double-s

22 lockage of PKC with its selective inhibitors bisindolylmaleimide and Goe 6976.

23 ilable small molecule LY-317615, a synthetic bisindolylmaleimide and inhibitor of protein kinase Cbet

24 In contrast, inhibition of PKC activity by bisindolylmaleimide and related compounds had no percept

25 nase C, however, was negated in studies with bisindolylmaleimide and Ro-31-8220, which, although comp

26 The hyperpermeability was corrected with bisindolylmaleimide and the selective PKCbeta inhibitor

27 A), and by the PKC inhibitors staurosporine, bisindolylmaleimide, and 1-O-hexadecyl-2-O-methylglycero

28 The PKC inhibitors staurosporine, bisindolylmaleimide, and AMG-C16 blocked the stimulated

29 were blocked by some PKC inhibitors (Go6976, bisindolylmaleimide, and Rottlerin), PKC-alpha, and PKC-

30 inhibited by the protein kinase C inhibitor bisindolylmaleimide, as well as the fungal metabolite br

31 The PKC inhibitor bisindolylmaleimide (BIM) abolished PDBu-mediated potent

32 The effects of PKC inhibition by bisindolylmaleimide (BIM) and protein synthesis inhibiti

33 itability was inhibited by the PKC inhibitor bisindolylmaleimide (BIM) I, but not by its inactive ana

34 by broad-spectrum PKC inhibitors, including bisindolylmaleimide (Bim) I.

35 tion of the EGFR at Tyr(1068) was blocked by bisindolylmaleimide (BIM), a PKC inhibitor, and rottleri

36 HX) and the protein kinase C (PKC) inhibitor bisindolylmaleimide (BIM), which both lowered FLIP and c

37 e Sepharose-linked protein kinase inhibitor, bisindolylmaleimide (BIM).

38 EK activation using the selective inhibitors bisindolylmaleimide (BIM, 1 microM) and PD98059 (30 micr

39 o-incubation of cells with the PKC inhibitor bisindolylmaleimide (BIM, 3 microM).

40 ined the structures of PIM-1 in complex with bisindolylmaleimide (BIM-1) and established the structur

41 Bisindolylmaleimide (BIM; a protein kinase C blocker), a

42 human melanocytes were first pretreated with bisindolylmaleimide (Bis), a selective PKC inhibitor, or

43 ects were abolished by ketanserin as well as bisindolylmaleimide (Bis-1), an inhibitor of PKC.

44 Bisindolylmaleimides (Bis) were originally described as

45 A specific PKC inhibitor, bisindolylmaleimide blocked the effect of ATPgammaS whil

46 y neurons was prevented by the PKC inhibitor bisindolylmaleimide but not by the phospholipase C inhib

47 pretreating cells with the pan-PKC inhibitor bisindolylmaleimide but not with the conventional PKC is

48 Protein kinase C inhibitors (bisindolylmaleimide, calphostin C) and inhibitors of mit

49 However, we found that bisindolylmaleimide compounds (which are also putative P

50 Structure-activity studies of bisindolylmaleimide compounds revealed that bisindolylma

51 In contrast, bisindolylmaleimide did not prevent cytokine secretion i

52 gel-stimulated fibroblasts were abrogated by bisindolylmaleimide GF 109203X and calphostin C, chemica

53 d protein kinase C (PKC), chelerythrine, and bisindolylmaleimide GF 109203X.

54 The PKC inhibitors calphostin C and bisindolylmaleimide GF109203X also abolished YT-mediated

55 Specific protein kinase C inhibitors (bisindolylmaleimide (GF109203X) and calphostin C) blocke

56 The bisindolylmaleimide, GF109203X (2-[1-(3-dimethylaminopro

57 ukemia cells to 17-AAG and the PKC inhibitor bisindolylmaleimide (GFX) did not result in enhanced let

58 The selective inhibitor of PKC, bisindolylmaleimide (GFX), mimicked NO action.

59 al inhibitors of protein kinase C, including bisindolylmaleimide (GFX), myristoylated PKC inhibitor p

60 B (25 muM) and enhanced by the PKC inhibitor bisindolylmaleimide I (1 muM).

61 Moreover, inhibition of PKC activity with bisindolylmaleimide I (BIM I) produced the same enhancin

62 Bisindolylmaleimide I (BIM), a protein kinase C signalin

63 ate MI-stage oocytes with the PKC inhibitor, bisindolylmaleimide I (BIM), transiently reduced (P < 0.

64 Reverse dialysis of the PKC inhibitors bisindolylmaleimide I (BIM; 30 microM) or chelerythrine

65 aMKII) inhibitor KN-62 and the PKC inhibitor bisindolylmaleimide I (BIMI), decreased HCO(3)(-) permea

66 the absence or presence of the PKC inhibitor bisindolylmaleimide I (Bis I) or the PKA inhibitor KT572

67 abolished by the protein kinase C inhibitor bisindolylmaleimide I (Bis I).

68 ect of PMA was blocked by the PKC inhibitors bisindolylmaleimide I (BIS; 100 nM) and chelerythrine ch

69 tive than the later one to pretreatment with Bisindolylmaleimide I (GF 109203X) (a protein kinase C i

70 Exposure to the PKC inhibitors bisindolylmaleimide I (GF I) or Ro-31-8220 converted osc

71 tested, only the protein kinase C inhibitor Bisindolylmaleimide I (GF109203X) caused dramatic protec

72 nd and could be blocked by the PKC inhibitor bisindolylmaleimide I (GF109203X).

73 IA binding were blocked by the PKC inhibitor bisindolylmaleimide I and by expression of a selective p

74 inhibited by the protein kinase C inhibitor bisindolylmaleimide I and by lowering Ca(2+) to nanomola

75 ctam V was antagonized by the PKC inhibitors bisindolylmaleimide I and Go 6976.

76 PKC inhibitor doses of bisindolylmaleimide I and Go-7874 that completely revers

77 secretion was inhibited by the PKC inhibitor bisindolylmaleimide I and inhibitors of the downstream k

78 The secretagogue action of PMA is blocked by bisindolylmaleimide I and is not very sensitive to the i

79 nsitization was blocked by the PKC inhibitor bisindolylmaleimide I and was not evoked by an inactive

80 Both Ro-31-8220 and bisindolylmaleimide I blocked the translocation of PKCal

81 Pretreatment of cells with bisindolylmaleimide I decreased PGF(2alpha)-stimulated p

82 In contrast, treatment with bisindolylmaleimide I did not affect the basal level of

83 Inhibition of PKC activity by bisindolylmaleimide I did not block lytic cycle activati

84 in kinase C (PKC) blockers staurosporine and bisindolylmaleimide I did not prevent inhibition, and th

85 Inhibition of PKC with bisindolylmaleimide I diminished cellular responses to e

86 Finally, the substrate-competitive inhibitor bisindolylmaleimide I displaces low affinity substrates

87 The potent PKC inhibitor bisindolylmaleimide I dose dependently inhibited ERK and

88 ort that pretreatment with the PKC inhibitor bisindolylmaleimide I enhanced PGF(2alpha)-stimulated IP

89 cked by PPADS, a protein kinase C inhibitor (bisindolylmaleimide I HCl), and actinomycin, an inhibito

90 Two inhibitors of PKC, namely, bisindolylmaleimide I hydrochloride (BM-1) and calphosti

91 the protein kinase C (PKC) inhibitors H7 or bisindolylmaleimide I induced an increase in the lifetim

92 PKC inhibitors Ro-31-8220 and bisindolylmaleimide I inhibited both PMA-induced PLD2 ph

93 phai, whereas the protein kinase C inhibitor bisindolylmaleimide I inhibited the response to both fML

94 effect of the PKC inhibitors Ro-31-8220 and bisindolylmaleimide I on PLD1 activation and found that

95 ening, whereas inhibition of PKC with either bisindolylmaleimide I or calphostin C caused a significa

96 i.c.v. administration of the PKC inhibitors bisindolylmaleimide I or Go6976 reversed the enhanced le

97 as reduced by treatment of cells with either bisindolylmaleimide I or UO126, inhibitors of PKC and MA

98 PKC inhibition with Ro-31-8425 or bisindolylmaleimide I sensitized this cell line to death

99 Co-administering either bisindolylmaleimide I with KT-5720, or Go-7874 with KT-5

100 ntal MCF-7 cells, PKC inhibitors (GF109203X (bisindolylmaleimide I) and staurosporine) reduced IRS-1

101 tion of PKC (inhibition by staurosporine and bisindolylmaleimide I).

102 uced phosphorylation of Nef was inhibited by bisindolylmaleimide I, a potent and specific inhibitor o

103 Pretreatment of the cells with bisindolylmaleimide I, a protein kinase C inhibitor, has

104 Bisindolylmaleimide I, a selective PKC inhibitor, blocke

105 on evidence that pretreatment of cells with bisindolylmaleimide I, a selective PKC inhibitor, or gel

106 In addition, bisindolylmaleimide I, a specific ATP-competitive protei

107 hosphorylated ZEBRA in vitro were blocked by bisindolylmaleimide I, a specific inhibitor of PKC.

108 ogue action of GnRH is not very sensitive to bisindolylmaleimide I, an inhibitor of protein kinase C,

109 2)-binding domain was inhibited by neomycin, bisindolylmaleimide I, and anti-type II PtdIns 5-phospha

110 ression as well as by the pan-PKC inhibitor, bisindolylmaleimide I, and by the mitogen-activated prot

111 C), because the PKC inhibitors calphostin C, bisindolylmaleimide I, and Go6976 blocked DR1/5-enhanced

112 ts of PDBu were blocked by the PKC inhibitor bisindolylmaleimide I, and they were not mimicked by the

113 hatidic acid (LPA) and their inhibition with bisindolylmaleimide I, as well as inhibition of RhoA and

114 ight of these, rottlerin, quercetin, K-252c, bisindolylmaleimide I, bisindolylmaleimide IX, U0126, in

115 lso abolished by treatment with 2 micrometer bisindolylmaleimide I, but [Ca(2+)](i) changes were unaf

116 inhibited by the protein kinase C inhibitor bisindolylmaleimide I, but not by the other protein kina

117 s with the competitive inhibitors Go 6983 or bisindolylmaleimide I, but not the uncompetitive inhibit

118 s inhibited by staurosporine, chelerythrine, bisindolylmaleimide I, calphostin C, and Ro31-8220 but n

119 The PKC-specific inhibitors bisindolylmaleimide I, calphostin C, CGP 41251, and the

120 ecific inhibitors, such as chelerythrine and bisindolylmaleimide I, did not reduce phagocytosis rates

121 e pre-treated i.c.v. with the PKC inhibitors bisindolylmaleimide I, Go-7874 or Go-6976, or with the m

122 abolished by the protein kinase C inhibitor bisindolylmaleimide I, partially abolished by the c-Jun-

123 e pan-specific PKC inhibitors RO 31-8220 and bisindolylmaleimide I, partially blocked by Go 6976, and

124 ed by select inhibitors of this kinase, i.e. bisindolylmaleimide I, Ro-32-0432, Go6983, and Rottlerin

125 these responses were not blocked by BAPTA or bisindolylmaleimide I, suggesting that these results may

126 vely by the PKC inhibitors staurosporine and bisindolylmaleimide I, whereas hSERT phosphorylation ind

127 e selective PKC inhibitors chelerythrine and bisindolylmaleimide I.

128 ration-dependent manner by the PKC inhibitor bisindolylmaleimide I.

129 not attenuated by a selective PKC inhibitor, bisindolylmaleimide I.

130 , or pharmacological suppression of PKC with bisindolylmaleimide I.

131 ersible in the presence of the PKC inhibitor bisindolylmaleimide I.

132 otein kinase C-specific inhibitor peptide or bisindolylmaleimide I.

133 otein kinase C-specific inhibitor peptide or bisindolylmaleimide I.

134 nhibited by the broad spectrum PKC inhibitor bisindolylmaleimide I.

135 l]-3-(1H-indol-3-yl)maleim ide], GF 109203X [bisindolylmaleimide I; 2-[1-(3-dimethylaminopropyl)indol

136 We conclude that bisindolylmaleimides I through III are some of the most

137 bisindolylmaleimide compounds revealed that bisindolylmaleimides I through III are the most potent n

138 uperoxide dismutase enzyme (100 units/ml) or bisindolylmaleimide-I (30 nmol/l) equally inhibited the

139 saline), which was significantly reduced by bisindolylmaleimide-I (P < 0.001 vs. glucose alone).

140 We suggest that bisindolylmaleimide-I acts by affecting either a pathway

141 lls with increasing concentrations of either bisindolylmaleimide-I or a peptide PKC pseudosubstrate i

142 In either case, the bisindolylmaleimide-I sensitivity of this pathway should

143 superfusion of the mesentery with 30 nmol/l bisindolylmaleimide-I, a potent, selective PKC inhibitor

144 sed by the protein kinase C (PKC) inhibitor, bisindolylmaleimide-I, but it did not reverse Wnt-1-indu

145 ted neutrophil adhesion was inhibited 50% by bisindolylmaleimide-I, implicating protein kinase C (PKC

146 The PKC-specific inhibitor bisindolylmaleimide II (BIM) (> or = 1 microM) antagoniz

147 ein kinase C (PKC) activity was blocked with bisindolylmaleimide II (BIM).

148 Pretreatment with the PKC inhibitor bisindolylmaleimide II (Bis II), with sucrose (0.4 m), o

149 cts of PMA were blocked by the PKC inhibitor bisindolylmaleimide II (Bis II).

150 cytisine) was also powerfully antagonized by bisindolylmaleimide II (IC(50) values of approximately 6

151 bation of the neurons with the PKC inhibitor bisindolylmaleimide II inhibits the effect of GPCR agoni

152 cked by co-treatment with the PKC inhibitor, bisindolylmaleimide II, and augmented by co-transfection

153 gonists failed to overcome the inhibition by bisindolylmaleimide II, suggesting noncompetitive nicoti

154 ocking the activity of protein kinase C with bisindolylmaleimide II.

155 KC) desensitization and by the PKC inhibitor bisindolylmaleimide, implicating PKC-linked activation o

156 Accordingly, the PKC inhibitor bisindolylmaleimide inhibited the oxidative burst induce

157 in PC-12 cells (IC(50) < or =37 nM), whereas bisindolylmaleimide IV and V have far less nicotinic ant

158 imide I, but not the uncompetitive inhibitor bisindolylmaleimide IV, prevents the dephosphorylation a

159 n, quercetin, K-252c, bisindolylmaleimide I, bisindolylmaleimide IX, U0126, indirubin, and indigo, in

160 3-(1H-indol-3-yl)maleimide], and Ro 31-8220 [bisindolylmaleimide IX; 2-{1-[3-(amidinothio)propyl]-1H-

161 er inhibitors of protein kinase C, including bisindolylmaleimide, K252a, H-7, and calphostin C, were

162 The conformation of a bisindolylmaleimide may be controlled by the size of a m

163 mbered macrocycles containing a N-N'-bridged bisindolylmaleimide moiety is described.

164 Neither bisindolylmaleimide nor Go6976, which block several prot

165 xpression and protein kinase C inhibition by bisindolylmaleimide on agonist-induced phosphorylation w

166 iciency, inhibition of protein kinase C with bisindolylmaleimide or calphostin C blocked resensitizat

167 is blocked by the protein kinase C inhibitor bisindolylmaleimide or protein tyrosine kinase inhibitor

168 logic inhibitors of PKC, such as Go 6983 and bisindolylmaleimide, or depletion of PKC delta by siRNA

169 and irreversible inhibition by calphostin C, bisindolylmaleimide, or rottlerin treatment versus activ

170 channel inhibition that was suppressed by a bisindolylmaleimide PKC inhibitor but not by a protein k

171 l 12-myristate 13-acetate or inhibition with bisindolylmaleimide prevented the DA-mediated increase i

172 ecanoyl phorbol 13-acetate and PKC inhibitor bisindolylmaleimide reciprocally down- and up-regulate,

173 The selective PKC inhibitor bisindolylmaleimide reduced phosphorylation of MARCKS-PS

174 Inhibition of protein kinase C by bisindolylmaleimide reduced the phosphorylation of both

175 The selective PKC enzyme inhibitor, bisindolylmaleimide, reduced PDB-stimulated AP-1 activit

176 de, and protein kinase C inhibitors, such as bisindolylmaleimide, rendered one of the resistant cell

177 an 18-h incubation with TPA or inhibition by bisindolylmaleimide resulted in profound inhibition of t

178 inhibitor mixture (staurosporine, genistein, bisindolylmaleimide, SB203580, and PD98059).

179 Nicotinic inhibition by bisindolylmaleimide seemed not to be readily reversible.

180 OCCM cells with the PKC inhibitor GF109203x (bisindolylmaleimide) significantly decreased mineralizat

181 part by the application of the PKC inhibitor bisindolylmaleimide, suggesting that the effect is media

182 FLIP), and was overcome by cycloheximide and bisindolylmaleimide, that specifically down-regulated FL

183 ntrast, the protein kinase C (PKC) inhibitor bisindolylmaleimide, the mitogen-activated protein kinas

184 e selective protein kinase C (PKC) inhibitor bisindolylmaleimide to determine the role of PKC in S6K

185 Treatment of the platelets with bisindolylmaleimide to inhibit protein kinase C prevente

186 Coapplication of bisindolylmaleimide V, used as a negative control compou

187 Thus, the use of agents such as bisindolylmaleimide VIII may be therapeutically useful f

188 Bisindolylmaleimide VIII potentiated Fas-mediated apopto

189 Administration of bisindolylmaleimide VIII to rats during autoantigen stim

190 Potentiation of Fas-mediated apoptosis by bisindolylmaleimide VIII was selective for activated, ra

191 duced by anti-Fas antibody in the absence of bisindolylmaleimide VIII, and in Jurkat and CEM-6 T cell

192 and MAPKAP-K1alpha) may be best inhibited by bisindolylmaleimides which adopt a compressed approximat

193 sites of S6K were specifically inhibited by bisindolylmaleimide, which also blocked integrin alpha2

194 cked by the protein kinase C (PKC) inhibitor bisindolylmaleimide, which reduced the extent of aggrega

195 constrast, GSK3beta may be best inhibited by bisindolylmaleimides whose ground state is a distorted s

196 1, ZEBRA, and Rta proteins were inhibited by bisindolylmaleimide X, a selective inhibitor of PKC.

197 ]-3-(1-methyl-1H-indo l-3-yl)maleimide, HCl, bisindolylmaleimide X, HCl), GRK2 [C-terminal GRK2 pepti