ライフサイエンスコーパス: tyrphostin

1 s inhibited by the tyrosine kinase inhibitor tyrphostin.

2 flavones and synthetic compounds such as the tyrphostins.

3 ellular signaling effects of isoflavones and tyrphostins.

4 than was membrane acid transport, except for tyrphostins.

5 Tyrphostin-1, an epidermal growth factor receptor (EGFR)

6 Preincubation with tyrphostin (20 microM; a potent and specific inhibitor o

7 the tyrosine kinase inhibitors genistein and tyrphostin 23 and their inactive analogues daidzein and

8 hosphatase inhibitor, reversed the effect of tyrphostin 23 on rapid endocytosis.

9 ment of bovine adrenal chromaffin cells with tyrphostin 23, a protein tyrosine kinase inhibitor, dram

10 wever, when HeLa cells were pre-treated with tyrphostin 23, a specific inhibitor of cellular epiderma

11 ant decrease in AAV-mediated transduction in tyrphostin 23-treated cells, whereas down-modulation of

12 AV transduction following pre-treatment with tyrphostin 23.

13 On the other hand, genistein, tyrphostin-25 (inhibitors of tyrosine-specific protein k

14 e PTK inhibitors genistein (1-30 microM) and tyrphostin 47 (0.1-10 microM).

15 Tyrphostin A-1, the inactive analog, was ineffective.

16 posing the cultures to 1 nmol/l genistein or tyrphostin A-23, the IP3 response to BK in the presence

17 Genistein and tyrphostin A-23, tyrosine kinase inhibitors, completely

18 Tyrphostin, a growth factor receptor/tyrosine kinase ant

19 combined with the inactive control compound tyrphostin A1 (100 microM) elicited significant (85%) ac

20 Tyrphostin A25 and controls, tyrphostin A1 and daidzein (a genistein congener), were

21 In contrast, treatment with tyrphostin A1 inhibited the tyrosine phosphorylation of

22 forms of these compounds (lavendustin B and tyrphostin A1) to provide negative controls.

23 23 and their inactive analogues daidzein and tyrphostin A1, respectively.

24 The tyrosine kinase inhibitor tyrphostin A10 inhibited CD22 movement at concentrations

25 An inhibitor of tyrosine kinase, i.e., tyrphostin A23 (100 microM), completely abolished EGF-ev

26 RME inhibitors Tyrphostin A23 and Endosidin 1 altered but did not block

27 sicular trafficking inhibitors Wortmannin or Tyrphostin A23 impaired flg22-elicited reactive oxygen s

28 For Tyrphostin A23, reduced flg22-induced reactive oxygen sp

29 rosine kinase inhibitors (tyrphostin AG1478, tyrphostin A23, tyrphostin A25, genistein) abolished bot

30 Tyrphostin A25 (TA25) and other tyrosine kinase inhibito

31 We find here, however, that tyrphostin A25 addition to mouse heart cytosol incubated

32 Tyrphostin A25 and controls, tyrphostin A1 and daidzein

33 tivation by LPA is additionally inhibited by tyrphostin A25 but not genistein or AG1478, indicating a

34 However, tyrphostin A25 did not inhibit NMB-stimulated increases

35 FN-f-stimulated increase in MMP-13, whereas tyrphostin A25 did not.

36 Genistein or tyrphostin A25 inhibited the production of NO in both LP

37 c extracts with the protein kinase inhibitor tyrphostin A25 results in enhanced transfer of methyl gr

38 hibitors (tyrphostin AG1478, tyrphostin A23, tyrphostin A25, genistein) abolished both oxyhb-induced

39 This effect was abrogated by wortmannin and tyrphostin A25, indicating the potential involvement of

40 The tyrosine kinase inhibitor, tyrphostin A25, inhibited NMB-induced phosphorylation of

41 ess fibers were inhibited by C3 transferase, tyrphostin A25, or dominant negative RhoA.

42 study examined the effects of genistein and tyrphostin A25, two potent inhibitors of PTKs, on the pr

43 Tyrphostin A25, which blocks activity of tyrosine kinase

44 cyte-enriched cultures was also inhibited by tyrphostin A25.

45 tile product and labeled protein occurs with tyrphostins A25, A47, and A51, but not with thirteen oth

46 We also examined the effect of Tyrphostin A46 (potent inhibitor of EGF-R and EGF-R kina

47 Tyrphostin A46 treatment significantly inhibited ulcer h

48 nhibitor) and the tyrosine kinase inhibitor, tyrphostin A47 (50 microm), but not its inactive analog,

49 nhibited by both PP2 and salicylate, whereas tyrphostin A47 failed to inhibit PYK2 tyrosine phosphory

50 After 30 min with ATP, tyrphostin A47 irreversibly inhibited hydrochloric acid

51 Tyrphostin A47 prevented all measurable tyrosine phospho

52 -2, 5-dihydroxycinnamate (erbstatin analog), tyrphostin A47, and lavendustin A, on thapsigargin-induc

53 d by Ro-31-8220, PP2, and salicylate but not tyrphostin A47.

54 47 (50 microm), but not its inactive analog, tyrphostin A63, also blocked AVP-stimulated Ca(2+) spiki

55 An inhibitor of tyrosine kinases, tyrphostin A63, also inhibited potentiation.

56 receptor 2 (TrkA/HER2) signaling; the other, tyrphostin A9 (A9), inhibits the platelet-derived growth

57 Tyrphostin A9 emerged as the most potent and selective o

58 Tyrphostin A9 inhibited TNF-induced tyrosine phosphoryla

59 fic small interfering RNA, or treatment with Tyrphostin A9 significantly blocked LPS-induced IL-8 pro

60 e tyrosine kinase inhibitors, genistein, and tyrphostin A9, a Pyk2-specific inhibitor, and piceatanno

61 y removal of extracellular calcium or by the tyrphostin A9, an I(CRAC) inhibitor.

62 The tyrosine kinase inhibitor tyrphostin A9, shown previously to block a PYK2-dependen

63 and the caspase-3 cleavage was attenuated by tyrphostin A9.

64 In contrast, tyrphostins A9 and AG126 act as mitochondrial uncouplers

65 Interactions between the tyrphostin adaphostin and proteasome inhibitors (eg, MG-

66 e binding-site-directed agent STI571 and the tyrphostin adaphostin are undergoing evaluation as bcr/a

67 ogether, these findings demonstrate that the tyrphostin adaphostin induces multiple perturbations in

68 phorylation of PDGF-R beta was attenuated by tyrphostin AG 1296, an inhibitor of PDGF-R kinase, sugge

69 by tyrosine kinase inhibitors (genistein and tyrphostin AG 1478) and potentiated by the tyrosine phos

70 bits growth factor receptor interactions, or tyrphostin AG 1478, a specific inhibitor of EGF receptor

71 r receptor (EGFR) tyrosine kinase inhibitor, tyrphostin AG 1478, were tested on three related human g

72 ermal growth factor (EGF) receptor inhibitor tyrphostin AG 1478.

73 f the cells with the specific Jak2 inhibitor tyrphostin AG 490 inhibits myeloid differentiation drive

74 =3.6 muM), NF 023 hydrate (IC50=6.2 muM) and tyrphostin AG 538 (IC50=3.6 muM).

75 Tyrphostin AG 556 improved survival times when compared

76 he rat T cell line Nb2-11c, we document that tyrphostin AG-490 blocked in vitro IL-2-induced cell pro

77 We recently reported that tyrphostin AG-490 selectively blocked IL-2 activation of

78 on, were treated immediately with one of two tyrphostins, AG 556 (n = 40) or AG 126 (n = 10), or with

79 nd the EGFR inhibitors erlotinib/tarceva and tyrphostin/AG-1478 are potent anti-cancer therapeutics.

80 cyanide p-trifluoromethoxyphenyl hydrazone, tyrphostins AG10 and AG18 increased the rate of oxygen c

81 Tyrphostin AG1024, a tyrosine kinase inhibitor of insuli

82 If tyrosine kinase inhibitors genistein and tyrphostin AG126 are included to prevent increased tyros

83 f catechol-O-methyltransferase activity with tyrphostin AG1288 prevents both base-volatile product fo

84 s and completely impaired in the presence of Tyrphostin AG1296, an inhibitor of PDGFR kinase.

85 lective inhibitor of PDGF-R kinase activity, tyrphostin AG1296.

86 to heal in organ culture in the presence of tyrphostin AG1478 (0-50 microM), a specific inhibitor of

87 ition of either EGFR or ERK activation, with tyrphostin AG1478 (1 microM) and PD 98059 (20 microM), r

88 The EGFr inhibitor, tyrphostin AG1478 (1 microM), inhibited both Bt2cAMP/AM-

89 An inhibitor of EGFr phosphorylation, tyrphostin AG1478 (1 microM), reversed CCh-stimulated ph

90 ells were allowed to heal in the presence of tyrphostin AG1478 (an EGFR inhibitor), GM6001 (a matrix

91 GF109203X (protein kinase C inhibitor), and tyrphostin AG1478 (epidermal growth factor receptor kina

92 Tyrphostin AG1478 also potentiated chloride secretory re

93 n of ERK, whereas the EGF receptor inhibitor tyrphostin AG1478 blocked basal and EGF-, but not PMA-,

94 ity, EGFR-expressing cells were treated with tyrphostin AG1478 EGFR inhibitor.

95 In organ culture experiments, tyrphostin AG1478 inhibited migration rates in a dose-de

96 he epidermal growth factor receptor-specific tyrphostin AG1478 inhibits GPCR-mediated Erk 1/2 activat

97 er specifically inhibiting ErbB1 (or 4) with tyrphostin AG1478 or ErbB2 with tyrphostin AG825.

98 Blockade of EGF receptor activation using tyrphostin AG1478 prevents H. pylori-mediated Ras activa

99 catalytic activity using the EGFR-selective tyrphostin AG1478 restored integrin alpha2 expression wi

100 Furthermore, inhibitors of EGFR (OSI-774 and Tyrphostin AG1478) selectively down-regulated these mole

101 mal growth factor receptor (EGFR) inhibitor (tyrphostin AG1478), a matrix metalloproteinase inhibitor

102 Chlorophenylamino)-6,7-dimethoxyquinazoline (Tyrphostin AG1478), a selective inhibitor of EGFR Tyr ki

103 expression of a dominant negative EGFR or by tyrphostin AG1478, a specific inhibitor for EGFR tyrosin

104 Both Tyrphostin AG1478, an EGFR tyrosine kinase inhibitor, an

105 both these and PKB activity were blocked by tyrphostin AG1478, an epidermal growth factor receptor-t

106 Tyrphostin AG1478, an inhibitor of the EGFR kinase, mark

107 hway by the specific EGF receptor inhibitor, tyrphostin AG1478, and the MEK inhibitor, PD098059, rest

108 was blocked by the pharmacological inhibitor tyrphostin AG1478, as well as by EGFR-neutralizing antib

109 response was blocked by the EGFR inhibitor, tyrphostin AG1478, implicating the EGFR in the pathway t

110 ayers and that the EGFR-selective inhibitor, tyrphostin AG1478, inhibited both EGF-stimulated and bas

111 The tyrphostin AG1478, known to inhibit EGF receptor phospho

112 ially sensitive to both the RGDS peptide and tyrphostin AG1478, suggesting that both focal adhesion a

113 g anti-HGF antibodies and the EGFR inhibitor tyrphostin AG1478, suggesting that EGFR ligands, togethe

114 ginosa in the presence of the EGFR inhibitor tyrphostin AG1478, the extracellular signal-regulated ki

115 A combination of tyrosine kinase inhibitors (tyrphostin AG1478, tyrphostin A23, tyrphostin A25, genis

116 dylinositol 3-kinase (PI3K) to the EGFr in a tyrphostin AG1478-sensitive manner.

117 d/or EGFR and by the EGFR-specific inhibitor tyrphostin AG1478.

118 s PD123319 was blocked also by GF109203X and tyrphostin AG1478.

119 ison suramin or the EGFR-selective inhibitor tyrphostin AG1478.

120 cific inhibitor of EGFR autophosphorylation, tyrphostin AG1478.

121 is(2-aminophenylthio) butadiene (U0126), and tyrphostin AG1478.

122 ls, blocked by an MMP inhibitor, GM6001, and tyrphostin AG1478.

123 Tyrphostins AG1478 (an epidermal growth factor receptor

124 tein, but not by the EGF receptor inhibitor, tyrphostin (AG1478).

125 he epidermal growth factor receptor-specific tyrphostin, AG1478 and by dominant negative mutants of m

126 Inhibition of EGFR activity with either the tyrphostin, AG1478, or blocking receptor-ligand interact

127 rmal growth factor receptor kinase inhibitor tyrphostin-AG1478, and re-expression was prohibited by t

128 (4.5 micromol/L), an AT(1) blocker, or with tyrphostin AG490 (5 micromol/L), an inhibitor of JAK 2 p

129 d leukocytes isolated from mice treated with tyrphostin AG490 are less adhesive on purified very late

130 treatment of T cell lines with high doses of tyrphostin AG490 have no effect on the viability, intrac

131 Hearts treated with the JAK 2 inhibitor tyrphostin AG490 showed a reduction in myocardial infarc

132 inhibit the expression of these proteins and tyrphostin AG490 to specifically block the activation of

133 Tyrphostin AG490, a specific inhibitor of Jak-2, signifi

134 Furthermore, the Janus kinase inhibitor, tyrphostin AG490, inhibited the constitutive activation

135 we show that the tyrosine kinase inhibitor, tyrphostin AG490, prevents binding of freshly isolated m

136 , and such activation could be attenuated by Tyrphostin AG538 (IGF-IR inhibitor), LY294002, or Wortma

137 hibited by mevalonate, a PI3K inhibitor, and tyrphostin AG538, suggesting roles for cholesterol and i

138 ed in proto-oncogene activation by asbestos, tyrphostin AG82 or herbimycin A was added to RPM cells b

139 growth factor receptor (HER)-2/neu inhibitor tyrphostin AG825 is preferentially toxic to PCa cells th

140 (or 4) with tyrphostin AG1478 or ErbB2 with tyrphostin AG825.

141 inase activity since treatment of cells with tyrphostin AG879 prevented serum-free media (SFM) induct

142 Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks

143 in (NSC680410), a small molecule congener of tyrphostin AG957, has been demonstrated previously to ha

144 Adaphostin (NSC 680410), an analog of the tyrphostin AG957, was previously shown to induce Bcr/abl

145 e decided to test the protective efficacy of tyrphostins against oxidative stress-induced nerve cell

146 These active tyrphostins all contain a catechol moiety and are good s

147 These tyrphostins also protect cells from hydrogen peroxide an

148 Tyrphostin, an inhibitor of the EGF receptor intrinsic t

149 d inhibition of p130(CAS) phosphorylation by tyrphostin and genistein, or expression of the substrate

150 Isoflavone, tyrphostin, and benzoquinonoid inhibitors were compared

151 avones, caffeic acid phenethyl ester (CAPE), tyrphostins, and curcumin confer inhibitory activity aga

152 Tyrphostins are a family of tyrosine kinase inhibitors o

153 We suggest that the methylated tyrphostins are further modified in the cell extract and

154 inhibited by the tyrosine kinase inhibitor, tyrphostin, as well as staurosporine.

155 Many commercially available tyrphostins, at concentrations ranging from 0.5 to 200 m

156 ine kinase inhibitors genistein (10 microM), tyrphostin B42 (10 microM) and herbimycin A (500 nM) all

157 In cell-attached recordings, the presence of tyrphostin B42 (10 microM) in the pipette solution activ

158 We have used tyrphostin B42 (AG490), a Jak-2 inhibitor, to determine

159 Treatment of the cells with genistein or tyrphostin B42 also decreased both EGF-stimulated PIP3 f

160 Treatment of mice with tyrphostin B42 also reduced the incidence and severity o

161 rine) but not by tyrosine kinase inhibitors (tyrphostin B42 and genistein).

162 In vivo treatment with tyrphostin B42 decreased the proliferation and IFN-gamma

163 e have further tested the in vivo effects of tyrphostin B42 in experimental allergic encephalomyeliti

164 Treatment of activated T cells with tyrphostin B42 inhibited the IL-12-induced tyrosine phos

165 These results suggest that tyrphostin B42 prevents EAE by inhibiting IL-12 signalin

166 ast, the inactive analogues of genistein and tyrphostin B42 were without effect.

167 nin prevented activation of KATP channels by tyrphostin B42.

168 oM) prevented the actions of both leptin and tyrphostin B42.

169 Treatment with tyrphostin B44 inhibited CCK-8-stimulated p130(Cas) phos

170 Various concentrations of lavendustin A and tyrphostin B46 were microinjected, as well as inactive f

171 Dose-response curves for lavendustin A, tyrphostin B46, and peptide A show clear inhibition of v

172 thway initiated by the methylation of select tyrphostins by endogenous catechol-O-methyltransferase.

173 ectivity demonstrated by the isoflavones and tyrphostins can serve as a pharmacophore for the design

174 lation of the ssD-BP, whereas treatment with tyrphostin causes dephosphorylation of the ssD-BP and co

175 or tyrosine kinase inhibitors (RTKIs) of the tyrphostin class that exhibit robust antiviral activity

176 have used tyrosine kinase inhibitors of the tyrphostin class to specifically block autophosphorylati

177 A series of isoflavone and tyrphostin compounds were found to inhibit the degradati

178 ed mitochondria to five structurally related tyrphostins demonstrated that their relative potencies a

179 However, genistein and tyrphostins did not produce chloride dependent effects.

180 Finally, the third group of tyrphostins does not appear to be effective as antioxida

181 5, A47, and A51, but not with thirteen other tyrphostin family members.

182 AG-490 is a member of the tyrphostin family of tyrosine kinase inhibitors.

183 ne kinase inhibitors (PTK, e.g., herbimycin, tyrphostin, genistein) blocked TNF-alpha-induced MCP-1 m

184 Because tyrphostins have chemical structures similar to those of

185 vation of the IGF-IR by EGF was inhibited by tyrphostin I-Ome-AG538, a tyrosine kinase inhibitor with

186 None of the tyrphostins, including A47, nor daidzein inhibited resor

187 Our data suggest that tyrphostin-induced alteration of stress response pathway

188 and an herbimycin-sensitive (genistein- and tyrphostin-insensitive) tyrosine kinase was required.

189 e found that glucose deprivation and various tyrphostins, known inhibitors of insulin-like growth fac

190 r potent Tdp1 inhibitors based on an initial tyrphostin lead compound 8.

191 yrosine kinase (EGF-R PTK) activity, such as tyrphostin, leads to significant augmentation of AAV tra

192 These findings suggest that the tyrphostin member has a broader spectrum of activity tha

193 Therefore, the effects of tyrphostins on cells are not limited to their ability to

194 ed the effect of tyrosine kinase inhibitors (tyrphostins) on survival.

195 treated with the kinase inhibitor genistein, tyrphostin, or staurosporine.

196 The tyrphostins protect nerve cells by three distinct mechan

197 AG1478, a tyrphostin selective for the EGF receptor, reduced the a

198 Tyrphostin stimulated rAAV transgene expression to a gre

199 e findings were interpreted as demonstrating tyrphostin stimulation of a novel type of protein carbox

200 n which removal of phenolic hydroxyls on the tyrphostin structure increased the potency for PDE1 and

201 Some tyrphostins, such as A25, act as antioxidants and elimin

202 tor XII, and the differential sensitivity to tyrphostin suggest that the EGF receptor and the factor

203 A or genistein (but not with either of three tyrphostins tested) significantly blocked TNF and NOS pr

204 Adaphostin is a tyrphostin that was originally intended to inhibit the B

205 emained in the single-strand conformation in tyrphostin-treated cells but double-stranded replicative

206 Northern analyses revealed that tyrphostin treatment enhanced mRNA accumulation more tha

207 binding characteristics were unchanged after tyrphostin treatment or adenovirus infection.

208 ivated protein kinase pathways revealed that tyrphostin treatment stimulated the activity of JNK and

209 gene expression which can be overcome by the tyrphostin treatment.

210 pression in lung epithelial cells (IB3) with tyrphostin treatment.

211 Effects of the tyrphostin tyrosine kinase inhibitor adaphostin (NSC 680

212 nic agonist carbachol, indicating that these tyrphostins uncouple mitochondria.

213 nazoline (AG1478), an EGF receptor-selective tyrphostin used at 1 microM, blocked EGF-induced NF-kapp

214 Various tyrphostins were also potent inhibitors of PDE1, PDE3, a

215 The four-carbon side chained tyrphostins were much less potent; however, a very inter