ライフサイエンスコーパス: herbimycin

1 -Arg-AL-Asp-Ser-Pro (GRADSP; 100 microM), or herbimycin A (0.1-10 nM) at 24 hours (sparse) or 7 days

2 in secretion since genistein (10 microM) and herbimycin A (1 microM), two tyrosine kinase inhibitors

3 quired protein tyrosine kinase activation as herbimycin A (10 micrograms/mL) blocked the affect of Fn

4 tors of pp60(Src), geldanamycin (62 nM), and herbimycin A (2.5 microM) blocked >50% of Raji prolifera

5 or genistein (75 micromol/L, 45 minutes) or herbimycin A (3 micromol/L, 45 minutes), tyrosine kinase

6 (10 microM), tyrphostin B42 (10 microM) and herbimycin A (500 nM) all resulted in activation of KATP

7 The ansamycin antibiotics, herbimycin A (HA) and geldanamycin (GM), bind to a conse

8 Phosphorylation is also inhibited by herbimycin A (IC50 < 1.0 microM) and staurosporine (IC50

9 porine (which inhibits protein kinase C) and herbimycin A (which inhibits protein tyrosine kinases),

10 of ROMK1 channels, because blocking PTK with herbimycin A abolished the inhibitory effect of c-Src on

11 However, herbimycin A abolished the inhibitory effect of PAO, ind

12 The tyrosine kinase inhibitor herbimycin A abolished the phosphorylation of p56lck and

13 ntly inhibited by the Src kinase inhibitors, herbimycin A and 4-amino-5-(4-methylphenyl)-7-(t-butyl)p

14 However, inhibition by herbimycin A and a catalytically inactive dominant negat

15 cific Src family tyrosine kinase inhibitors (herbimycin A and CP-118,556) blocked BMK1 activation by

16 with the protein tyrosine kinase inhibitors herbimycin A and genistein completely blocks S6K activat

17 We applied the tyrosine kinase inhibitors herbimycin A and genistein to whole 40% grasshopper embr

18 sodium azide and tyrosine kinase inhibitors herbimycin A and genistein, and with soluble detergent-e

19 Protein tyrosine kinase (PTK) inhibitors, herbimycin A and genistein, prevented gp60-activated mac

20 as the selective tyrosine kinase inhibitors, herbimycin A and genistein.

21 d activation, was sensitive to inhibition by herbimycin A and insensitive to inhibition by increased

22 by applying inhibitors of cytoplasmic PTKs, herbimycin A and lavendustin A, to intact brain preparat

23 The effects of herbimycin A and PAO were absent in oocytes expressing t

24 Moreover, protein tyrosine kinase inhibitor herbimycin A and PLC inhibitor U73122 both blocked CD43-

25 Significantly, both herbimycin A and PP2 abrogated ouabain-induced but not e

26 ty to respond to cytokines were resistant to herbimycin A and staurosporine.

27 by addition of the tyrosine kinase inhibitor herbimycin A and was delayed by the phosphatidylinositol

28 In cardiac myocytes and A7r5 cells, herbimycin A antagonized the ouabain-induced increase in

29 in expression by serum and its repression by herbimycin A are regulated at the level of mRNA translat

30 ew is further reinforced by the finding that herbimycin A can prevent the onset of programmed cell de

31 The tyrosine kinase inhibitors genistein and herbimycin A caused concordant reductions in Fc gamma R-

32 The protein tyrosine kinase inhibitor herbimycin A completely eliminated the protective effect

33 Tyrosine kinase inhibition by herbimycin A diminished J393/CD43-mediated apoptosis, wh

34 ble Mer protein or tyrosine kinase inhibitor herbimycin A effectively blocked the effects of protein

35 The bcr/abl kinase-selective inhibitor herbimycin A increased the induction of nuclear apoptosi

36 Conversely, herbimycin A increased the proportion of low voltage-act

37 expressing the bcr/abl oncoprotein and that herbimycin A increases induction of programmed cell deat

38 OV-3 cells with the inhibitors genestein and herbimycin A indicated that tyrosine kinases were involv

39 ontaining antibiotics geldanamycin (GDA) and herbimycin A inhibit Hsp90 function in vitro at low micr

40 Treatment with herbimycin A inhibited Cot activity in the MEK/ERK pathw

41 ein-tyrosine kinase inhibitors genistein and herbimycin A inhibited TGF-beta1-induced protein tyrosin

42 treatment with the tyrosine kinase inhibitor herbimycin A inhibited this response.

43 Furthermore, the effect of herbimycin A is absent in the oocytes pretreated with ei

44 Preincubation of RAW 264.7 cells with herbimycin A or genistein (but not with either of three

45 Inhibition of tyrosine kinases with herbimycin A or genistein protected against the TSP-indu

46 RFL-6 cells treated in cell culture with herbimycin A or genistein, inhibitors of protein tyrosin

47 inase C inhibitors or with the PTK inhibitor herbimycin A or PP1 resulted in reduced Src PTK activity

48 I 3-kinase, are refractory to the effects of herbimycin A or serum starvation on D-cyclin expression.

49 tor tyrosine kinase inhibitors genistein and herbimycin A or with the phosphatidylinositol 3-kinase (

50 the tyrosine kinase inhibitors genistein or herbimycin A prevented VEGF/VPF-induced permeability.

51 ondrial changes, Colo-205 cells treated with herbimycin A produced increased levels of reactive oxyge

52 In addition, herbimycin A produced pathfinding errors in which many l

53 lar gap formation, whereas pretreatment with herbimycin A protected against this effect.

54 rosine kinase (PTK) inhibitors genistein and herbimycin A reduced M. tuberculosis-stimulated PLD acti

55 Herbimycin A repression is characterized by a decrease i

56 ein-tyrosine kinase inhibitors genistein and herbimycin A resulted in a concentration-dependent inhib

57 sp90 inhibitors geldanamycin, radicicol, and herbimycin A resulted in a dose-dependent suppression of

58 of cells with the tyrosine kinase inhibitor herbimycin A resulted in an inhibition of receptor ubiqu

59 Suppression of PTK by herbimycin A significantly attenuated the inhibitory eff

60 Furthermore, herbimycin A suppressed the phosphorylation of AKT and E

61 orphonuclear leukocytes were pretreated with herbimycin A to determine the role of protein tyrosine k

62 eased when cells were pretreated with either herbimycin A to induce cytosolic Hsp70 or with an inhibi

63 Addition of herbimycin A to keratocytes exposed to TGFbeta showed a

64 The addition of either genistein or herbimycin A to RAW 264.7 cell cultures 1-6 It after sti

65 The ability of herbimycin A to sensitize K562, TOM 1 or KCL-22 cells to

66 K activity was not significantly affected by herbimycin A treatment and, under these conditions, FAK

67 ng with an antiphosphotyrosine antibody, and herbimycin A treatment failed to inhibit p65 phosphoryla

68 e activation by asbestos, tyrphostin AG82 or herbimycin A was added to RPM cells before exposure to a

69 Inhibition of PLD activity by genistein or herbimycin A was associated with inhibition of phagocyto

70 tein tyrosine kinase inhibitor (genistein or herbimycin A) was added after internalization of the org

71 Herbimycin A, a drug that binds to Hsp90, induces the de

72 Addition of herbimycin A, a potent pp60src tyrosine-kinase inhibitor

73 channels was not affected in the presence of herbimycin A, a PTK inhibitor, and was larger in rats th

74 ne phosphorylation in cells was inhibited by herbimycin A, a relatively specific inhibitor for member

75 ays were required for iNOS induction because herbimycin A, a tyrosine kinase inhibitor, and 4-(4-fluo

76 itor for p70(RSK), but could be inhibited by herbimycin A, a tyrosine kinase inhibitor, and partially

77 Herbimycin A, a tyrosine kinase inhibitor, and SP600125,

78 Herbimycin A, a tyrosine kinase inhibitor, induces cellu

79 In contrast, treatment with herbimycin A, a tyrosine kinase inhibitor, inhibited MIP

80 osporine, inhibitors of protein kinase C, or herbimycin A, an inhibitor of nonreceptor tyrosine kinas

81 Addition of 1 microm herbimycin A, an inhibitor of PTK, had no significant ef

82 Moreover, application of herbimycin A, an inhibitor of PTK, increased K(+) curren

83 NA and protein synthesis, and was blocked by herbimycin A, an inhibitor of S pi protein tyrosine kina

84 nt that can be blocked by preincubation with herbimycin A, an inhibitor of tyrosine kinases.

85 , the tyrosine kinase inhibitors, genistein, herbimycin A, and 4-amino-5-(4-chlorophenyl)-7-(t-butyl)

86 inhibited by the tyrosine kinase inhibitor, herbimycin A, and binding activity was eliminated by tyr

87 rs of tyrosine kinases such as genistein and herbimycin A, and the immunosuppressant cyclosporin A.

88 1) The tyrosine kinase inhibitor, herbimycin A, and the specific Src kinase family inhibit

89 eased [Ca2+]i was inhibited by thapsigargin, herbimycin A, and U73122, but only partially reduced by

90 is blocked by the tyrosine kinase inhibitor, herbimycin A, as well as by an inhibitor of endocytosis,

91 ct tyrosine kinase inhibitors, genistein and herbimycin A, as well as microinjection of a monoclonal

92 of p23 buffered the effects of radicicol and herbimycin A, but not novobiocin, on AhR signaling.

93 tivation was demonstrated by inhibition with herbimycin A, but not with the Src inhibitor PP1 or over

94 by the cytoplasmic tyrosine kinase inhibitor herbimycin A, but that of IK,S and IK,I was unaffected,

95 nhibited by blocking cell proliferation with herbimycin A, demonstrating that Src kinase activity can

96 The tyrosine kinase inhibitor, herbimycin A, eliminated the suppression of proteolysis

97 n inhibitor of src-related tyrosine kinases, herbimycin A, inhibited increases of collagenase messeng

98 the tyrosine kinase inhibitors genistein and herbimycin A, moreover, was marginal at best.

99 not detected in nuclei of cells treated with herbimycin A, suggesting that its appearance depends on

100 In RFL-6 cells treated with herbimycin A, the increase in MnSOD-BP activity was asso

101 In the presence of herbimycin A, the pCC growth cone was redirected across

102 Geldanamycin or herbimycin A, tyrosine kinase inhibitors, blocked HBV re

103 w that the ansamysin drugs, geldanamycin and herbimycin A, which inhibit the assembly of some signali

104 . risticii was not inhibited by genistein or herbimycin A, which suggests that these reagents did not

105 Based on the effects of herbimycin A, wortmannin, and chelerythrine on iC5b67-in

106 um ([Ca2+]i) elevation was also inhibited by herbimycin A, wortmannin, and PP2.

107 Our results show that a herbimycin A- and staurosporine-sensitive phase of CDK4

108 in loss from CD4(+) and CD8(+) T cells via a herbimycin A-sensitive pathway(s) presumably involving o

109 teract with cell-surface GAGs to transduce a herbimycin A-sensitive signal which, over a period of se

110 a-independent pathway indicates a role for a herbimycin A-sensitive tyrosine kinase.

111 in vivo Grb2 binding to Shc was observed in herbimycin A-treated fibroblasts after FN stimulation.

112 inases by 24-h pretreatment with 0.25 microM herbimycin A.

113 s of the N-terminal inhibitors radicicol and herbimycin A.

114 he addition of the tyrosine kinase inhibitor herbimycin A.

115 of collagenase by IL-1 was also inhibited by herbimycin A.

116 d up to 90% by the tyrosine kinase inhibitor herbimycin A.

117 locked by the Src kinase-selective inhibitor herbimycin A.

118 or tyrosine kinase inhibitors genistein and herbimycin A.

119 18 tail was attenuated by an NRTK inhibitor, herbimycin A; a phosphatidylinositol 3'-kinase (PI 3-kin

120 The activity at 500 mosmol/kg was reduced by herbimycin, a tyrosine kinase inhibitor and by 5,6-dichl

121 duced hypertrophic response by genistein and herbimycin-A indicated a requirement for protein tyrosin

122 Finally, catalase or herbimycin-A inhibition of constitutive or hydrogen pero

123 ttle effect on V7-mediated inhibition, while herbimycin, an inhibitor of tyrosine kinase, synergizes

124 Distinct sensitivity profiles to genistein, herbimycin and 8-Br-cAMP biochemically distinguished mov

125 Consistent with this, herbimycin and geldanamycin pretreatment of human umbili

126 Herbimycin and genistein inhibited bone resorption with

127 with the tyrosine protein kinase-antagonists herbimycin and genistein.

128 Although both herbimycin and staurosporine blocked agrin-induced AChR

129 Moreover, two tyrosine kinase inhibitors, herbimycin and staurosporine, that blocked beta-subunit

130 e benzoquinoid ansamycins geldanamycin (GA), herbimycin, and their derivatives are emerging as novel

131 The tyrosine kinase inhibitor herbimycin blocked Ad19-induced IL-8 expression.

132 In membrane incubated with inhibitors, the herbimycin effect also inhibited Cl- transport by variab

133 ited by a protein tyrosine kinase inhibitor, herbimycin, in a dose-dependent manner, suggesting that

134 uding shear stress, the response to which is herbimycin-inhibitable.

135 genistein and the benzoquinonoid antibiotic herbimycin inhibited hydrochloric acid transport with 50

136 ked agrin-induced AChR phosphorylation, only herbimycin inhibited the phosphorylation of MuSK.

137 the tyrosine kinase inhibitors genistein or herbimycin inhibited the rapid mobilization of calcium i

138 le an inhibitor of tyrosine phosphorylation (herbimycin) inhibited the increase in cPLA2 activation a

139 vii) The specific tyrosine kinase inhibitor, herbimycin, or Src family kinase inhibitor, PP1, abolish

140 In contrast, herbimycin protected Philadelphia-negative HL60 cells fr

141 The concentration of herbimycin required to synergize with etoposide was simi

142 nhibition when PKC was downregulated; and an herbimycin-sensitive (genistein- and tyrphostin-insensit

143 ERK1/2 via a shared pathway that involves an herbimycin-sensitive tyrosine kinase and PKC.

144 Ultrastructural examination of herbimycin-treated cells demonstrated morphologic featur

145 Both genistein and herbimycin (tyrosine kinase inhibitors) suppressed the e

146 otein tyrosine kinase inhibitors (PTK, e.g., herbimycin, tyrphostin, genistein) blocked TNF-alpha-ind

147 Enhancement of nuclear apoptosis by herbimycin was not attributable to downregulation of the

148 of [PP]2-InsP4, whereas a similar inhibitor, herbimycin, was without effect.