ライフサイエンスコーパス: ICI 182,780

1 This effect was blocked by fluvestrant (ICI 182,780).

2 by a specific estrogen receptor antagonist (ICI 182,780).

3 tration with an estrogen receptor inhibitor (ICI 182,780).

4 t the AP-1 site is augmented by fulvestrant (ICI 182,780).

5 ffect that was reversed by the E2 antagonist ICI 182 780.

6 receptor antagonist JB1 or the ER antagonist ICI 182,780.

7 rew in the presence of the pure antiestrogen ICI 182,780.

8 PI-9 was not induced by raloxifene or ICI 182,780.

9 essed by antiestrogens such as tamoxifen and ICI 182,780.

10 r different SERMs, and the pure antiestrogen ICI 182,780.

11 reversed by the estrogen receptor antagonist ICI 182,780.

12 and neuroprotection by DHPG was abolished by ICI 182,780.

13 lls that have survived prolonged exposure to ICI 182,780.

14 only partially blocked by the ER antagonist ICI 182,780.

15 and were not observed with the antiestrogen ICI 182,780.

16 enuated in the presence of the ER antagonist ICI 182,780.

17 t blocked by the estrogen receptor inhibitor ICI 182,780.

18 ked by an estrogen receptor (ER) antagonist, ICI 182,780.

19 he conventional estrogen receptor antagonist ICI 182,780.

20 blocked by the estrogen receptor antagonist ICI 182,780.

21 anscription with ER-alpha that is blunted by ICI 182,780.

22 d by E2 in a manner that was counteracted by ICI 182,780.

23 activity is blocked by the pure antiestrogen ICI 182,780.

24 ogenic responsiveness to both raloxifene and ICI 182,780.

25 K activity, are blocked by the anti-estrogen ICI 182,780.

26 tatic subline was unaffected by estrogen and ICI 182,780.

27 nd not by tamoxifen or the pure antiestrogen ICI 182,780.

28 ddition of the estrogen receptor antagonist, ICI 182,780.

29 moxifen and the estrogen receptor antagonist ICI 182,780.

30 y can be inhibited by 4-hydroxytamoxifen and ICI 182,780.

31 mRNAs that were blocked by the antiestrogen ICI 182,780.

32 zed a more potent estrogen receptor blocker, ICI 182,780.

33 estrogen and blocked by estrogen antagonist ICI 182,780.

34 ated by the estrogen receptor down-regulator ICI 182,780.

35 is mediated by ERalpha and reversed by E2 or ICI 182,780.

36 revented by the estrogen receptor antagonist ICI 182,780.

37 of ERalpha on Ser-118 that was inhibited by ICI 182,780.

38 e they were blocked by the pure antiestrogen ICI 182,780.

39 be blocked completely by the antiestrogenic ICI 182,780.

40 7beta-E2 or the estrogen receptor antagonist ICI 182,780.

41 sitivity to the antiproliferative effects of ICI 182,780.

42 r cells compared to raloxifene, tamoxifen or ICI-182,780.

43 adiol, analogs of tamoxifen, raloxifene, and ICI-182,780.

44 han 1000-fold compared with ER liganded with ICI-182,780.

45 nists with ER affinity comparable to that of ICI-182,780.

46 not blocked by 100-fold excess tamoxifen or ICI-182,780.

47 amoxifen, but not by the complete antagonist ICI 182, 780.

48 294002, and the estrogen receptor antagonist ICI 182, 780.

49 ) were infused with vehicle (35% ethanol) or ICI 182 780 (0.1-3.0 microg min(-1)) into one uterine ar

50 egnancy (late pregnant ewes) were also given ICI 182 780 (0.23-2.0 microg (ml uterine blood flow)-1;

51 atory rises in UBF reached near peak levels, ICI 182 780 (1 or 2 microg (ml uterine blood flow)-1) wa

52 The presence of the nuclear ER antagonist, ICI 182,780 (1 microM), not only failed to block all 3 m

53 mide (1 microg ml(-1)) or the anti-oestrogen ICI 182,780 (1 microM).

54 We recently discovered that ICI 182,780 (1), an antagonist of estrogen receptor (ER)

55 on by E2 was suppressed by the ER antagonist ICI 182,780 (10 mum) or by inhibition of transcription (

56 These alterations were eliminated by ICI 182,780 (10(-7) mol/L), an estrogen receptor antagon

57 Moreover, both tamoxifen (10(-6) M) and ICI-182,780 (10(-6) M) function as agonists for VEGF in

58 fically antagonized by the receptor blockers ICI 182,780 (200 nM) and RU486 (15 nM), respectively.

59 oxalin-1-one; 10 mg/kg] or an ER antagonist (ICI 182,780; 3 mg/kg) 30 minutes before E2 (100 microg/k

60 n of IRS-1 was blocked with the antiestrogen ICI 182,780; (3) nuclear IRS-1 colocalized and co-precip

61 or without an estrogen receptor antagonist (ICI 182,780), a PI3K inhibitor (Wortmannin), or vehicle,

62 ithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist.

63 This study used ICI 182,780, a nonselective ER antagonist, to test the h

64 makes tamoxifen (TAM), but not raloxifene or ICI 182,780, a potent inducer of PI-9.

65 Topical treatments with ICI 182,780, a pure estrogen receptor antagonist, caused

66 of both 17beta-estradiol and E2-BSA, whereas ICI 182,780, a selective inhibitor of the nuclear estrog

67 o the ERalpha in a manner similar to that of ICI-182,780, a pure ER antagonist.

68 Lastly, the ER antagonist ICI 182,780 abrogates ERK activation and the anti-apopto

69 In late pregnant sheep ICI 182 780 also mildly and acutely (for 5-30 min) eleva

70 We now show for the first time that ICI 182,780 also exhibits potent antiprogestin activity

71 Additionally, the combination of ICI 182,780 also sensitizes MCF-7 and T47D cell lines to

72 ction was blocked by the receptor antagonist ICI 182,780, also prevented by inhibitors of NOS1 (7-nit

73 both 17beta-estradiol and E(2)-BSA, whereas ICI 182,780, an inhibitor of the nuclear ER, had no effe

74 ncubation of the vessels with 17beta-E2 plus ICI, 182,780, an estrogen receptor antagonist, or wortma

75 interaction was blocked by the ER antagonist ICI 182,780 and by Ptox.

76 dothelial cells; this response is blocked by ICI 182,780 and by the eNOS inhibitor Nomega-nitro-L-arg

77 ced neuroprotection, but coadministration of ICI 182,780 and each single molecule exerted a comparabl

78 lin, or eNOS cofactors, which was blocked by ICI 182,780 and ERalpha antibody.

79 ICI 182,780 and JB1 blocked the IGF-I-induced increases

80 effects were inhibited by the ER antagonist ICI 182,780 and prevented by inhibition of gene transcri

81 ed by the estrogen receptor (ER) antagonists ICI 182,780 and tamoxifen, and from ERalpha(-/-) bone ma

82 Both nonselective ER antagonism with ICI 182,780 and the inhibition of gene transcription wit

83 blocked by an estrogen receptor antagonist (ICI 182,780) and by a Trx reductase inhibitor (azelaic a

84 nyl]nonyl]estra-1,3,5(10)-tri ene-3,17-diol (ICI 182,780)] and the ER-alpha- and ER-beta-specific ago

85 (ERalpha) and reversed by the anti-estrogen ICI 182, 780, and this response was not affected by prog

86 sed by an estrogen receptor (ER) antagonist, ICI 182,780, and by phospho-inositide-3 kinase inhibitor

87 not by the estrogen receptor (ER) antagonist ICI 182,780, and did not appear to result from estradiol

88 posure to 17beta-estradiol, the antiestrogen ICI 182,780, and estrogenic pollutants on coronary vascu

89 ted by the estrogen receptor (ER) antagonist ICI 182,780, and siRNA-mediated silencing of ER expressi

90 blocked by the estrogen receptor antagonist ICI 182,780, and the intracellular Ca2+ chelator 1,2-bis

91 roperties of the steroidal pure antiestrogen ICI 182,780 are not affected by the D351Y ER.

92 The pure antiestrogen ICI 182,780 binds to the estrogen receptor with high aff

93 The coadministration of ICI 182,780 blocked the effects of DDT.

94 howed that LY117018 increased transport, and ICI 182,780 blocked the effects of LY117018, delineating

95 Inclusion of the pure estrogen antagonist ICI 182,780 blocked the increase in luciferase activity

96 ICI 182,780 blocked the increase in synapse density.

97 antiestrogens, trans 4'-hydroxytamoxifen and ICI 182,780, blocked the elevation of BRCA1 and BRCA2 mR

98 ucibility with either ER-alpha or -beta, and ICI 182,780 blocks activation by ER-alpha but not by ER-

99 The ER antagonist ICI 182,780 blocks this effect.

100 ICI 182,780 blunted the E2-related protective effect and

101 creased the reactivity of the raloxifene- or ICI 182,780-bound ERalpha, with probes that recognize th

102 nhibited by the estrogen receptor antagonist ICI 182,780 but could be provoked using non-cell membran

103 2) inhibit the antiproliferative activity of ICI 182,780 but not of 2ME(2).

104 d not only by the ER antagonist fulvestrant (ICI 182,780) but also by JNJ 16259685, and neuroprotecti

105 In contrast, the pure antiestrogen ICI 182,780 causes a dramatic reduction of the ER protei

106 tingly, treatment of the MCF-7:2A cells with ICI 182,780 causes a slight increase in ER mRNA, which i

107 The antiestrogen fulvestrant (ICI 182,780) causes immobilization of estrogen receptor-

108 ed for this activity, because the antagonist ICI 182,780 completely blocked the inhibitory activity o

109 Estrogen receptor antagonism with ICI 182,780 completely inhibited estrogen-mediated eNOS

110 10 nM concentration of the pure antiestrogen ICI 182,780 could not inhibit 1 nM estradiol- or diethyl

111 The same concentration of ICI 182,780 decreased PRL secretion to 1% of estradiol-

112 d-type ER, it has previously been shown that ICI 182,780 decreases ER only at the protein level.

113 In Ovx sheep, local infusion of ICI 182 780 did not alter systemic cardiovascular parame

114 or the classic estrogen-receptor antagonist ICI 182,780 did not alter testosterone-induced changes.

115 iprogestin activity in this test system, and ICI 182,780 did not inhibit the activity of transfected

116 he estrogen receptor antagonist fulvestrant (ICI 182,780) did not block effects of 17beta-E2, but inc

117 The estrogen receptor antagonist, ICI 182,780, did not block protection by 17beta-E(2).

118 Moreover, the estrogen antagonist ICI 182,780 does not inhibit the antiproliferative activ

119 The specific inhibitors to ER (ICI 182,780), EGF receptor (EGFR; AG1478), and mitogen-a

120 18 phosphorylation in response to estradiol, ICI 182,780, epidermal growth factor (EGF), and phorbol

121 reatment of mice with the pure ER antagonist ICI 182 780 (faslodex) inhibited gene expression respons

122 was inhibited by 4-hydroxytamoxifen (4-OHT), ICI 182 780 (Faslodex), and siRNA ER alpha indicating th

123 ss active than ZOHT or the pure antiestrogen ICI 182,780 (faslodex) in stimulating transcription from

124 he estrogen receptor antagonist fulvestrant (ICI-182,780, Faslodex) but was unaffected by inhibitors

125 The estrogen receptor (ER) antagonist ICI 182,780 fully reversed the effects of the hormone on

126 Moreover, we found that the addition of ICI 182,780 (Fulvestrant), a selective ER down-regulator

127 -beta-estradiol (E2), the pure ER antagonist ICI 182,780 (fulvestrant, Faslodex), or epidermal growth

128 beta-methyl-cyclodextrin, the ER antagonist ICI 182,780 [fulvestrant (Faslodex)], and two inhibitors

129 ICI 182,780 had no effect on E2 inhibition of constituti

130 These results clearly establish that ICI 182,780 has significant antiprogestin activity in ad

131 The antiestrogens tamoxifen and ICI 182,780 have been portrayed as competitive antagonis

132 The full ER antagonist, ICI 182 780 (ICI) had no effect.

133 recently demonstrated that the ER antagonist ICI 182,780 (ICI) acts as an ER agonist in uterus of mic

134 activity, whereas raloxifene allows less and ICI 182,780 (ICI) allows none.

135 droxytamoxifen (TOT) and raloxifene (Ral) or ICI 182,780 (ICI) and by estradiol (E2) in estrogen rece

136 examine the effects of the pure antiestrogen ICI 182,780 (ICI) on various targets of IGF-I signaling

137 vide evidence that a complete ER antagonist, ICI 182,780 (ICI), as well as a selective ER modulator,

138 porter gene was blocked by the ER antagonist ICI 182,780 (ICI), demonstrating the presence of functio

139 tructurally distinct AE, tamoxifen (TAM) and ICI 182,780 (ICI), significantly inhibited the prolifera

140 icromolar 4-hydroxytamoxifen and fulvestrant/ICI 182,780 (ICI).

141 s were blocked by the specific ER-antagonist ICI 182,780 (ICI, 10(-5) M), confirming estrogen specifi

142 treated with the nonselective ER antagonist ICI 182,780 (ICI; 0.5, 1.5, or 5 mg. kg(-1). d(-1), subc

143 s from that of 4-hydroxy-tamoxifen (4HT) and ICI-182,780 (ICI).

144 y blocked by 100 nmol/L of pure antiestrogen ICI 182,780, implying estrogen receptor (ER) dependence

145 The estrogen receptor (ER) antagonist ICI 182,780 improved survival in female mice infected wi

146 es could be repressed by estrogen antagonist ICI 182 780 in MCF-7 cells yet were enhanced in SKBR3 ce

147 2 were differentially regulated by E2 versus ICI 182,780 in 201T and 273T NSCLC cell lines.

148 selectively blocked by the pure antiestrogen ICI 182,780 in a dose-dependent manner.

149 of estradiol was observed with tamoxifen or ICI 182,780 in any of the yeast models employed.

150 The efficacy of ICI 182,780 in control PC12 cells may have been due to t

151 cells, but CRE activity is not regulated by ICI 182,780 in either responsive or resistant cells.

152 Although IRF-1 mRNA expression is induced by ICI 182,780 in sensitive cells, this regulation is lost

153 nt with 17beta-estradiol that was blunted by ICI 182,780 in the nonmetastatic variant.

154 The ER blocker ICI 182,780 increases the concentration of des-(1-3)IGF-

155 blocked by the estrogen receptor antagonist, ICI 182,780, indicating that estrogen receptor is requir

156 hed in the presence of the pure antiestrogen ICI 182,780, indicating that the classic estrogen recept

157 Importantly, the ICI 182,780-induced antiproliferative effects were rever

158 ion; rather, dominant-negative IRF-1 reduces ICI 182,780-induced apoptosis.

159 A dominant-negative IRF-1 eliminates the ICI 182,780-induced apoptotic response (reduced >4-fold)

160 models of elevated endogenous E2beta, local ICI 182 780 infusion inhibited the elevated UBF seen in

161 -nonylphenol, o.p'-DDT, and the antiestrogen ICI 182,780 inhibit L-type Ca2+ channels in vascular smo

162 ns, whereas 4(OH)-tamoxifen, raloxifene, and ICI-182,780 inhibit these interactions.

163 ICI 182,780 inhibited progesterone-induced gene transcri

164 ICI 182 780 is a pure steroidal oestrogen receptor (ER)

165 In addition, the pure antiestrogen ICI 182,780 is capable of inhibiting EM-652-induced TGF-

166 Inhibition of NFkappaB activity by ICI 182,780 is lost in resistant cells, but CRE activity

167 gen activity of compounds like tamoxifen and ICI 182,780 is not caused by their ability to competitiv

168 Because a pure anti-ER ICI 182,780 is not only able to suppress the up-regulati

169 By comparison, ICI 182,780 is the more effective cell growth inhibitor.

170 vely unstable ER.ERE complex, and binding of ICI-182,780 leads to slow formation (ka is approximately

171 ct through the hormone binding site, whereas ICI 182,780 may cause receptor activation through an all

172 ICI 182,780 may therefore have therapeutic benefit in NS

173 with the selective estrogen receptor blocker ICI 182,780 mimicked the deficit in S-M behaviors caused

174 effects of treatment with the anti-estrogen ICI 182,780 on CXCR4-mediated tumor growth.

175 to investigate the effects of tamoxifen and ICI 182,780 on ER dimerization, transcriptional activati

176 erence in the effects of TAM, raloxifene and ICI 182,780 on immunosurveillance in breast cancer.

177 ding has eliminated the effects of 4-OHT and ICI 182,780 on the steady-state ER77 protein level.

178 ) and antiestrogens (4-hydroxy-tamoxifen and ICI-182,780) on PC-3 and DU-145 cells.

179 Co-treatment with ER antagonists ICI 182,780 or 4-hydroxytamoxifen blocked resveratrol- o

180 Cotreatment with antiestrogens (ICI 182,780 or 4-hydroxytamoxifen) antagonized the effec

181 Blocking ER with ICI 182,780 or mGluR1a with LY 367385 prevented ERalpha

182 concomitant treatment with the antiestrogen ICI 182,780 or the protein synthesis inhibitor cyclohexi

183 Co-administration of ICI 182,780 or Wortmannin abolished beneficial effects o

184 Coadministration of ICI 182,780 or Wortmannin abolished the beneficial effec

185 ntly induced by genistein in the presence of ICI 182,780 or wortmannin, indicating a dependence on ph

186 Administration of ICI-182,780 or cycloheximide failed to influence these e

187 An estrogen receptor antagonist, ICI-182,780, or E2 failed to inhibit uterine LF gene exp

188 By contrast, the ER antagonist ICI 182,780 overcame the inhibitory effect of estrogen.

189 ith or without estrogen receptor antagonist (ICI 182,780), PI3K inhibitor (Wortmannin), or vehicle wa

190 17alpha-Estradiol failed to protect, and ICI 182,780 prevented E2 from protecting against cell de

191 Coadministration of ICI 182,780 prevented those salutary effects of flutamid

192 ol (E2)-dependent and was nearly absent when ICI 182,780, raloxifene, or 4-hydroxytamoxifen were boun

193 gene expression and support a model in which ICI 182,780 reduces proliferation of NSCLC cells via its

194 atment with the estrogen receptor antagonist ICI 182,780 rescued TH-ir cells.

195 In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS

196 n E2 in mediating this desensitization in an ICI 182, 780-sensitive manner in both guinea pig and mou

197 d osteosarcoma model cancer cell lines in an ICI 182,780-sensitive manner.

198 ol induced suppression, and the antiestrogen ICI 182,780 stimulated transcription of the AP1 reporter

199 a-catenin in MC3T3-E1 cells was inhibited by ICI 182,780, suggesting that an estrogen receptor is req

200 was diminished in NRL-PRL males treated with ICI 182,780, suggesting that PRL enhances ER-mediated gr

201 h the PFKFB3 inhibitor and the anti-estrogen ICI 182,780 synergistically induces apoptotic cell death

202 iption in the presence of 17 beta-estradiol, ICI 182,780, tamoxifen, raloxifene, genistein, or daidze

203 entially are more resistant to tamoxifen and ICI-182,780 than cells that express an equivalent or hig

204 igands to elicit ERK phosphorylation, and of ICI 182,780 to block the actions of estradiol in ERKO cu

205 ER ligands 17beta-estradiol, raloxifene, and ICI 182,780 to effectively block the cell death-inducing

206 ddition of the estrogen receptor antagonist, ICI 182,780, to influence the extent of cell death induc

207 displace the estradiol from the ER, whereas ICI 182,780 treatment resulted in a 4-fold increase in [

208 ase ER protein levels to a similar extent as ICI 182,780 treatment, and, in addition, EM-652 has no e

209 I-9 mRNA induction, whereas the antiestrogen ICI 182, 780 was a pure antagonist.

210 ls in media containing the pure antiestrogen ICI 182,780 was also markedly inhibited upon induction o

211 The antiprogestin activity of ICI 182,780 was detected in HeLa, HepG2, and CV1 cells t

212 Tamoxifen and ICI 182,780 were able to induce ER dimerization and ER-d

213 Remarkably, the antiestrogens tamoxifen and ICI 182,780, were shown both in vitro and in vivo studie

214 nscriptional activation was fully blocked by ICI 182,780, whereas the specific ERbeta antagonist RR-t