ライフサイエンスコーパス: hydroxytamoxifen

1 -fold (estradiol) to approximately 4-fold (4-hydroxytamoxifen).

2 ues than the larger ligands (P1496 and trans-hydroxytamoxifen).

3 e the agonist and antagonist activities of 4-hydroxytamoxifen.

4 uced or eliminated the agonist activity of 4-hydroxytamoxifen.

5 orders of magnitude lower than that of alpha-hydroxytamoxifen.

6 s sensitive to a well known ER antagonist, 4-hydroxytamoxifen.

7 estrogen receptor domain are treated with 4-hydroxytamoxifen.

8 is activated when the cells are exposed to 4-hydroxytamoxifen.

9 e estrogen receptor that selectively binds 4-hydroxytamoxifen.

10 ndothelial deletion of Gpx4 was induced by 4-hydroxytamoxifen.

11 d by one of two synthetic ligands, CMP8 or 4-hydroxytamoxifen.

12 p27 protein following c-Myc activation by 4-hydroxytamoxifen.

13 tional unless associated with tamoxifen or 4-hydroxytamoxifen.

14 mation of group II adducts did not involve 4-hydroxytamoxifen.

15 in vivo after treatment with tamoxifen or 4-hydroxytamoxifen.

16 e human estrogen receptor, is activated by 4-hydroxytamoxifen.

17 e of tamoxifen, N-desmethyl-tamoxifen, and 4-hydroxytamoxifen.

18 of Cre recombinase, which is activated by 4-hydroxytamoxifen.

19 mpletely dependent on ectopic provision of 4-hydroxytamoxifen.

20 ced by systemic or local administration of 4-hydroxytamoxifen.

21 splicing activities that highly depend on 4-hydroxytamoxifen.

22 ethylene glycols to an E and Z mixture of 4-hydroxytamoxifen.

23 adiol and increased antagonist activity of 4-hydroxytamoxifen.

24 estradiol and the mixed agonist/antagonist 4-hydroxytamoxifen.

25 l and decreased the antagonist activity of 4-hydroxytamoxifen.

26 Administration of 4-hydroxytamoxifen 2 weeks after birth activates the expre

27 le and efficient two-step synthesis of (Z)-4-hydroxytamoxifen (2a).

28 ceptor alpha by the addition or removal of 4-hydroxytamoxifen (4-HT), we show that IFN-gamma, CD122,

29 nd addition of the membrane-permeable drug 4-hydroxytamoxifen (4-HT), which binds to the ER domain, l

30 ndent on the cell-permeable small molecule 4-hydroxytamoxifen (4-HT).

31 lowing us to control its dimerization with 4-hydroxytamoxifen (4-HT).

32 By contrast, covalent binding of 4-hydroxytamoxifen (4-OH-tam) was 3-5-fold higher than tha

33 hylstilbestrol (DES), tamoxifen (TAM), and 4-hydroxytamoxifen (4-OHT) as high-affinity ligands for ER

34 re continuously treated with the ER ligand 4-hydroxytamoxifen (4-OHT) to allow tumor formation.

35 4-Hydroxytamoxifen (4-OHT), a selective estrogen receptor

36 agonist-bound state, the ERRgamma LBD with 4-hydroxytamoxifen (4-OHT), and the ERRgamma LBD with 4-OH

37 When ER was liganded by the antiestrogen 4-hydroxytamoxifen (4-OHT), COUP-TF-half-site interaction

38 duced reduction in miR-21 was inhibited by 4-hydroxytamoxifen (4-OHT), ICI 182 780 (Faslodex), and si

39 The active metabolite of tamoxifen, 4-hydroxytamoxifen (4-OHT), is used in the laboratory for

40 mations by administration or withdrawal of 4-hydroxytamoxifen (4-OHT), respectively.

41 phorylation of c-Src, which was blocked by 4-hydroxytamoxifen (4-OHT), suggesting that E2 activated c

42 ith synthetic estrogenic compounds such as 4-hydroxytamoxifen (4-OHT), tamoxifen, and diethylstilbest

43 Here we report that 4-hydroxytamoxifen (4-OHT), with an EC(50) of ~1.7 nM, inc

44 factor (COUP-TF)-I interacts directly with 4-hydroxytamoxifen (4-OHT)- and estradiol (E(2))-occupied

45 e generated transgenic mice that express a 4-hydroxytamoxifen (4-OHT)-dependent switchable c-myc onco

46 we engineered a knock-in allele encoding a 4-hydroxytamoxifen (4-OHT)-inducible telomerase reverse tr

47 an be regulated by provision or removal of 4-hydroxytamoxifen (4-OHT).

48 etabolites (N-desmethyl tamoxifen [N-DMT], 4-hydroxytamoxifen [4-OHT], and 4-hydroxy-N-desmethyl-tamo

49 e that the selective ER modulators (SERMs) 4-hydroxytamoxifen (4HT) and raloxifene are able to elevat

50 ), synergistically restores sensitivity to 4-hydroxytamoxifen (4HT) in resistant MCF7/RR and MCF7/LCC

51 ditional zebrafish model of T-ALL in which 4-hydroxytamoxifen (4HT) treatment induces MYC activation

52 ls in the presence of the synthetic ligand 4-hydroxytamoxifen (4HT), thereby indicating that STAT3ER

53 ivation in carcinogenesis, mice expressing 4-hydroxytamoxifen (4HT)-activated ROCK2 (K14.ROCK(er)) we

54 A2 with its C terminus fused in frame to a 4-hydroxytamoxifen (4HT)-dependent mutant estrogen recepto

55 ibited by the hydroxylated TAM derivative, 4-hydroxytamoxifen (4HTAM), although this derivative was l

56 xifen has biologically active metabolites: 4-hydroxytamoxifen (4OHT) and endoxifen.

57 alleles encoding a fusion between p53 and 4-hydroxytamoxifen (4OHT) receptor (p53ER(TAM)).

58 op/flox tdTomato reporter mice and applied 4-hydroxytamoxifen (4OHT) to back skin at postnatal day (P

59 topical treatment with the inducing agent 4-hydroxytamoxifen (4OHT), ODC activity and putrescine lev

60 nist activity of 17beta-estradiol (E2) and 4-hydroxytamoxifen (4OHT), on an estrogen response element

61 (TPEs), which are structurally similar to 4-hydroxytamoxifen (4OHT), were used for mechanistic studi

62 lly mature adult epidermis, we expressed a 4-hydroxytamoxifen (4OHT)-regulated Ras fusion in transgen

63 adult epidermis by topical application of 4-hydroxytamoxifen (4OHT).

64 All TPEs were estrogenic and, unlike 4-hydroxytamoxifen (4OHTAM) and Endoxifen, induced cell gr

65 ls and exposed them to a cytotoxic dose of 4-hydroxytamoxifen (4OHTAM).

66 (2)-induced Ca(2+) responses because E(2), 4-hydroxytamoxifen (activates GPR30), and G-1, but not DES

67 expression was regulated by the timing of 4-hydroxytamoxifen administration.

68 better than inhibition by the antiestrogen 4-hydroxytamoxifen alone, whereas a combination of both RA

69 When alpha-hydroxytamoxifen (alpha-OHTAM) was incubated with rat li

70 This enabled the separation of alpha-hydroxytamoxifen and 4-hydroxytamoxifen, which were not

71 Estrogen receptor antagonists 4-hydroxytamoxifen and 7alpha-[9-(4,4, 5,5,5-pentafluoro-p

72 4-Hydroxytamoxifen and alpha-hydroxytamoxifen appear to be

73 strongly in combination with letrozole or 4-hydroxytamoxifen and fulvestrant.

74 dy substantial proliferation in micromolar 4-hydroxytamoxifen and fulvestrant/ICI 182,780 (ICI).

75 Two different antiestrogens, trans 4'-hydroxytamoxifen and ICI 182,780, blocked the elevation

76 and that this activity can be inhibited by 4-hydroxytamoxifen and ICI 182,780.

77 a binding affinity of 2.5% relative to E/Z-4-hydroxytamoxifen and inhibits the growth of four breast

78 traductally administered anticancer agents 4-hydroxytamoxifen and pegylated liposomal doxorubicin (PL

79 ed an in vitro system in which some SERMs (4-hydroxytamoxifen and resveratrol) demonstrate estrogenic

80 Microsomal activation of 4-hydroxytamoxifen and tamoxifen, respectively, in the pre

81 nduced in human keratinocytes treated with 4-hydroxytamoxifen, and its activation triggered loss of m

82 HCl transport was inhibited by tamoxifen, 4-hydroxytamoxifen, and the calmodulin antagonists, triflu

83 ion was reversibly inhibited by tamoxifen, 4-hydroxytamoxifen, and trifluoperazine with IC50 values o

84 eatment with antiestrogens (ICI 182,780 or 4-hydroxytamoxifen) antagonized the effects of 17beta-estr

85 4-Hydroxytamoxifen and alpha-hydroxytamoxifen appear to be the proximate metabolites

86 sary to accumulate and strip tamoxifen and 4-hydroxytamoxifen are discussed.

87 trogen agonist (estradiol) and antagonist (4-hydroxytamoxifen) are reduced.

88 st cancer drug tamoxifen and a metabolite, 4-hydroxytamoxifen, as the target analytes.

89 ifen resistant and were induced to grow by 4-hydroxytamoxifen, as well as other antiestrogens, as par

90 eatment with ER antagonists ICI 182,780 or 4-hydroxytamoxifen blocked resveratrol- or E(2)-induced MA

91 The anti-estrogen 4-hydroxytamoxifen blocks Rsk2-mediated activation of ERal

92 induced by the partial estrogen antagonist 4-hydroxytamoxifen, but not by the complete antagonist ICI

93 ng Raloxifene, Diethylstilbestrol, E2, and 4-hydroxytamoxifen, by employing FLuc-based optical biolum

94 osteoclasts to study effects of tamoxifen, 4-hydroxytamoxifen, calmodulin antagonists, estrogen, diet

95 ion doubling times in estrogen-depleted or 4-hydroxytamoxifen containing medium.

96 ansgenic zebrafish that express ubiquitous 4-hydroxytamoxifen-controlled Cre recombinase activity fro

97 nt expression of ERbeta and treatment with 4-hydroxytamoxifen decreased tumorigenic potential of thes

98 RAB-PAX3-HBD protein and showed it to be a 4-hydroxytamoxifen-dependent transcriptional repressor of

99 gand-binding domain of ERalpha allowed for 4-hydroxytamoxifen-dependent, synergistic activation of mb

100 so acquire resistance to the anti-estrogen 4-hydroxytamoxifen due to the rise of cyclin D1 levels in

101 nces activation function-1 activity in the 4-hydroxytamoxifen-ERalpha complex with the complete loss

102 adiol (E(2))-ERalpha (IC(50) 9 microm) and 4-hydroxytamoxifen-ERalpha-mediated gene expression.

103 DOX-TEG-TAM retains 60% of the affinity of 4-hydroxytamoxifen for AEBS.

104 cell lines, the nonsteroidal antiestrogen 4-hydroxytamoxifen has little effect on the mRNA level but

105 Addition of the antiestrogen 4-hydroxytamoxifen (HT) alone did not increase the T(M); h

106 is presented that the estrogen antagonist 4-hydroxytamoxifen (HT) can occupy not only the core bindi

107 QR is up-regulated by the antiestrogen trans-hydroxytamoxifen in breast cancer cells.

108 a Myc-estrogen receptor fusion protein by 4-hydroxytamoxifen in mouse cells resulted in suppression

109 low nanomolar levels of both tamoxifen and 4-hydroxytamoxifen in pristine solution and 1/10 diluted u

110 activated in vivo by the administration of 4-hydroxytamoxifen in time release pellets.

111 the potential to activate tamoxifen to alpha-hydroxytamoxifen, in addition to that occurring in the s

112 (2)) and two antiestrogens, raloxifene and 4-hydroxytamoxifen, in estrogen receptor alpha (ERalpha)-p

113 e activation mechanism(s) of tamoxifen and 4-hydroxytamoxifen, in vivo adducts were compared by 32P-p

114 Exposure to 4-hydroxytamoxifen induced Cre-mediated recombination in o

115 udies reveal that stimulation of MER-Akt1 by hydroxytamoxifen induces GLUT1 mRNA and protein accumula

116 ith immobility at approximately 30 d after 4-hydroxytamoxifen injection.

117 4-Hydroxytamoxifen is a full agonist at a transforming gro

118 ion 3, consistent with the hypothesis that 4-hydroxytamoxifen is a precursor for adduct fraction 3 in

119 ely minor DNA adduct of tamoxifen (dG-N(2)-4-hydroxytamoxifen) is more mutagenic than the major tamox

120 n to be induced by the synthetic estrogen, 4-hydroxytamoxifen, leading to regulated activation of a b

121 Activation of STAT6:ER* by 4-hydroxytamoxifen leads to specific activation of STAT6-r

122 Selection for resistance to 4-hydroxytamoxifen led to the development of the SUM44/LCC

123 led that in vitro fractions 3 and Q1 (from 4-hydroxytamoxifen) matched the major in vivo group I addu

124 revention to investigate how tamoxifen and 4-hydroxytamoxifen may act in normal human mammary epithel

125 Activating PKB with 4-hydroxytamoxifen mimicked insulin by decreasing mTOR rea

126 , tamoxifen, and the tamoxifen metabolites 4-hydroxytamoxifen, N-desmethyltamoxifen, and endoxifen.

127 methodology include tamoxifen, raloxifene, 4-hydroxytamoxifen, nafoxidine, and idoxifene.

128 ctors that interact with ER complexed with 4-hydroxytamoxifen (OHT) at natural target genes in a huma

129 findings that tamoxifen and its derivative 4-hydroxytamoxifen (OHT) can exert estrogen receptor-indep

130 ER chimeras are conditionally activated by 4-Hydroxytamoxifen (OHT) in a dose-dependent manner.

131 ions of tamoxifen or its active metabolite 4-hydroxytamoxifen (OHT) induce estrogen receptor alpha (E

132 We show that tamoxifen and 4-hydroxytamoxifen (OHT) promoted cell cycle progression o

133 adiol, catecholestrogens, the antiestrogen 4-hydroxytamoxifen (OHT), and dietary flavonoids.

134 e show that TAM and its active metabolite, 4-hydroxytamoxifen (OHT), can actively induce programmed c

135 beta-Estradiol (E(2)) or the antiestrogen, 4-hydroxytamoxifen (OHT), induce apoptosis in stably trans

136 lpha LBD bound to the selective antagonist 4-hydroxytamoxifen (OHT).

137 in the presence of the synthetic steroid, 4-hydroxytamoxifen (OHT).

138 induced by estrogen, moxestrol (MOX), and 4-hydroxytamoxifen (OHT).

139 inimal promoters, these regulators provide 4-hydroxytamoxifen- or RU486-inducible expression systems

140 tivation of exogenous AML1 (RUNX1)-ER with 4-hydroxytamoxifen prevents inhibition of G1 progression m

141 s incubated with alpha-acetoxytamoxifen or 4-hydroxytamoxifen quinone methide (4-OHtamQM) to generate

142 s of tamoxifen, alpha-acetoxytamoxifen and 4-hydroxytamoxifen quinone methide (4-OHtamQM).

143 Tamoxifen, but not 4-hydroxytamoxifen, rapidly induced apoptosis in p53(-) HM

144 rn on the Akt kinase cascade, we expressed a hydroxytamoxifen-regulatable form of Akt (myristoylated

145 survival of Rat-1 fibroblasts containing a 4-hydroxytamoxifen-regulated c-Myc allele, c-MycER, after

146 either sensitive (parental) or resistant (4-hydroxytamoxifen-resistant (OHT(R))) to tamoxifen showed

147 to generate dG-N(2)-tamoxifen and dG-N(2)-4-hydroxytamoxifen, respectively.

148 rmed cells by the addition of tamoxifen or 4-hydroxytamoxifen resulted in apoptosis.

149 In the presence of 4-hydroxytamoxifen STAT3-ER was translocated in the nucleu

150 models for tamoxifen resistance; that is, 4-hydroxytamoxifen-stimulated MCF7ERalphaHA cells that ove

151 1)) in the Hepa1c1c7 cells; we verified that hydroxytamoxifen stimulates MER-Akt1 activity to a simil

152 y low concentrations of antiestrogens (trans-hydroxytamoxifen, tamoxifen, and ICI182,780) in estrogen

153 data support the hypothesis that uptake of 4-hydroxytamoxifen targeted doxorubicin-formaldehyde conju

154 on of three different agonists but not trans-hydroxytamoxifen (the only ligand lacking a second hydro

155 ted by 500 nmol/L raloxifene or 500 nmol/L 4-hydroxytamoxifen, these concentrations of antiestrogens

156 BD ARMS cell lines and were implanted with 4-hydroxytamoxifen timed-release pellets exhibited suppres

157 potentiated the action of the antiestrogen 4-hydroxytamoxifen to inhibit the growth of T-47D cells.

158 Systemic time-release implant delivery of 4-hydroxytamoxifen to severe combined immunodeficient mice

159 bicin-formaldehyde conjugate targeted, via 4-hydroxytamoxifen, to the estrogen receptor (ER) and anti

160 timulation and inhibition by the SERMs trans-hydroxytamoxifen (TOT) and raloxifene (Ral) or ICI 182,7

161 ative stress enzymes is upregulated by trans-hydroxytamoxifen (TOT) in breast epithelial cell lines p

162 In the presence of ERbeta, trans-hydroxytamoxifen (TOT) protects cells against 17beta-est

163 Antiestrogens, such as trans-hydroxytamoxifen (TOT), have partial agonistic activity

164 as promoted by E2 and the antiestrogen trans-hydroxytamoxifen (TOT).

165 d the endogenous p57 promoter in response to hydroxytamoxifen treatment in the presence of cyclohexim

166 The antiestrogen trans-hydroxytamoxifen was a partial agonist for PI-9 mRNA ind

167 , whereas a combination of both RAD001 and 4-hydroxytamoxifen was most effective.

168 AICD induced by TGF-beta1, providing that 4-hydroxytamoxifen was present.

169 pithelial proliferative response to E2 and 4-hydroxytamoxifen was retained in the AA/-females, and ut

170 a Myc-estrogen receptor fusion protein by 4-hydroxytamoxifen was sufficient to repress gas1 gene tra

171 The targeting group, E/Z-4-hydroxytamoxifen, was selected for its ability to tightl

172 hat lack B- and C-rings, hexestrol and trans-hydroxytamoxifen, was unaffected.

173 zyme that adds O-GlcNAc) can be induced by 4-hydroxytamoxifen, we screened the expression of 84 HSPs

174 ly absent when ICI 182,780, raloxifene, or 4-hydroxytamoxifen were bound to the ERs.

175 ogenous cyclin D3 mRNA upon treatment with 4-hydroxytamoxifen, which induces nuclear accumulation of

176 R1-amplified cell lines show resistance to 4-hydroxytamoxifen, which is reversed by small interfering

177 e separation of alpha-hydroxytamoxifen and 4-hydroxytamoxifen, which were not resolvable in methanol

178 Chemical oxidation of 4-hydroxytamoxifen with silver(II) oxide, followed by incu

179 96, and the partial agonist-antagonist trans-hydroxytamoxifen) with those that are predicted to conta

180 that observed for the ER partial agonist, 4-hydroxytamoxifen (ZOHT).