ライフサイエンスコーパス: bisindolylmaleimide I

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

2 , or pharmacological suppression of PKC with bisindolylmaleimide I.

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

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

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

6 nhibited by the broad spectrum PKC inhibitor bisindolylmaleimide I.

7 e selective PKC inhibitors chelerythrine and bisindolylmaleimide I.

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

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

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

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

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

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

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

15 Bisindolylmaleimide I, a selective PKC inhibitor, blocke

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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