ライフサイエンスコーパス: 4-hydroxytamoxifen

1 3-fold (estradiol) to approximately 4-fold (4-hydroxytamoxifen).

2 ple the agonist and antagonist activities of 4-hydroxytamoxifen.

3 educed or eliminated the agonist activity of 4-hydroxytamoxifen.

4 duced by systemic or local administration of 4-hydroxytamoxifen.

5 was sensitive to a well known ER antagonist, 4-hydroxytamoxifen.

6 ne estrogen receptor domain are treated with 4-hydroxytamoxifen.

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

8 ine estrogen receptor that selectively binds 4-hydroxytamoxifen.

9 or p27 protein following c-Myc activation by 4-hydroxytamoxifen.

10 nctional unless associated with tamoxifen or 4-hydroxytamoxifen.

11 ormation of group II adducts did not involve 4-hydroxytamoxifen.

12 ed in vivo after treatment with tamoxifen or 4-hydroxytamoxifen.

13 gen receptor-positive breast cancer cells to 4-hydroxytamoxifen.

14 endothelial deletion of Gpx4 was induced by 4-hydroxytamoxifen.

15 ted by one of two synthetic ligands, CMP8 or 4-hydroxytamoxifen.

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

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

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

19 completely dependent on ectopic provision of 4-hydroxytamoxifen.

20 ng splicing activities that highly depend on 4-hydroxytamoxifen.

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

22 tradiol and increased antagonist activity of 4-hydroxytamoxifen.

23 o estradiol and the mixed agonist/antagonist 4-hydroxytamoxifen.

24 iol and decreased the antagonist activity of 4-hydroxytamoxifen.

25 Administration of 4-hydroxytamoxifen 2 weeks after birth activates the exp

26 mple and efficient two-step synthesis of (Z)-4-hydroxytamoxifen (2a).

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

28 and addition of the membrane-permeable drug 4-hydroxytamoxifen (4-HT), which binds to the ER domain,

29 pendent on the cell-permeable small molecule 4-hydroxytamoxifen (4-HT).

30 allowing us to control its dimerization with 4-hydroxytamoxifen (4-HT).

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

32 ethylstilbestrol (DES), tamoxifen (TAM), and 4-hydroxytamoxifen (4-OHT) as high-affinity ligands for

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

34 Prx1creER-egfp;td-Tomato mice and delivered 4-hydroxytamoxifen (4-OHT) to the mouse calvaria, subper

35 acrylic acid (GW7604) as a derivative of (Z)-4-hydroxytamoxifen (4-OHT) was linked by diaminoalkane s

36 4-Hydroxytamoxifen (4-OHT), a selective estrogen recepto

37 e agonist-bound state, the ERRgamma LBD with 4-hydroxytamoxifen (4-OHT), and the ERRgamma LBD with 4-

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

39 induced reduction in miR-21 was inhibited by 4-hydroxytamoxifen (4-OHT), ICI 182 780 (Faslodex), and

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

41 ormations by administration or withdrawal of 4-hydroxytamoxifen (4-OHT), respectively.

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

43 with synthetic estrogenic compounds such as 4-hydroxytamoxifen (4-OHT), tamoxifen, and diethylstilbe

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

45 n factor (COUP-TF)-I interacts directly with 4-hydroxytamoxifen (4-OHT)- and estradiol (E(2))-occupie

46 we generated transgenic mice that express a 4-hydroxytamoxifen (4-OHT)-dependent switchable c-myc on

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

48 can be regulated by provision or removal of 4-hydroxytamoxifen (4-OHT).

49 nables cell proliferation in the presence of 4-hydroxytamoxifen (4-OHT).

50 metabolites (N-desmethyl tamoxifen [N-DMT], 4-hydroxytamoxifen [4-OHT], and 4-hydroxy-N-desmethyl-ta

51 ate that the selective ER modulators (SERMs) 4-hydroxytamoxifen (4HT) and raloxifene are able to elev

52 ls), synergistically restores sensitivity to 4-hydroxytamoxifen (4HT) in resistant MCF7/RR and MCF7/L

53 onditional zebrafish model of T-ALL in which 4-hydroxytamoxifen (4HT) treatment induces MYC activatio

54 ells in the presence of the synthetic ligand 4-hydroxytamoxifen (4HT), thereby indicating that STAT3E

55 ctivation in carcinogenesis, mice expressing 4-hydroxytamoxifen (4HT)-activated ROCK2 (K14.ROCK(er))

56 BNA2 with its C terminus fused in frame to a 4-hydroxytamoxifen (4HT)-dependent mutant estrogen recep

57 nhibited by the hydroxylated TAM derivative, 4-hydroxytamoxifen (4HTAM), although this derivative was

58 moxifen has biologically active metabolites: 4-hydroxytamoxifen (4OHT) and endoxifen.

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

60 stop/flox tdTomato reporter mice and applied 4-hydroxytamoxifen (4OHT) to back skin at postnatal day

61 rogen receptor modulators (SERMs), including 4-hydroxytamoxifen (4OHT), activate AF-1 preferentially

62 er topical treatment with the inducing agent 4-hydroxytamoxifen (4OHT), ODC activity and putrescine l

63 gonist activity of 17beta-estradiol (E2) and 4-hydroxytamoxifen (4OHT), on an estrogen response eleme

64 es (TPEs), which are structurally similar to 4-hydroxytamoxifen (4OHT), were used for mechanistic stu

65 tally mature adult epidermis, we expressed a 4-hydroxytamoxifen (4OHT)-regulated Ras fusion in transg

66 s after inflammasome activation induced with 4-hydroxytamoxifen (4OHT).

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

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

69 ells and exposed them to a cytotoxic dose of 4-hydroxytamoxifen (4OHTAM).

70 Notably, intradermal injection of 4-hydroxytamoxifen activated oncogene cassettes in vivo,

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

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

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

74 Two different antiestrogens, trans 4'-hydroxytamoxifen and ICI 182,780, blocked the elevati

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

76 4-Hydroxytamoxifen and alpha-hydroxytamoxifen appear to

77 lethylene bisphenol (BPTPE), and antagonists 4-hydroxytamoxifen and endoxifen.

78 n of HNRNPA2/B1 reduced MCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role fo

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

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

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

82 h a binding affinity of 2.5% relative to E/Z-4-hydroxytamoxifen and inhibits the growth of four breas

83 intraductally administered anticancer agents 4-hydroxytamoxifen and pegylated liposomal doxorubicin (

84 oped an in vitro system in which some SERMs (4-hydroxytamoxifen and resveratrol) demonstrate estrogen

85 Microsomal activation of 4-hydroxytamoxifen and tamoxifen, respectively, in the p

86 induced in human keratinocytes treated with 4-hydroxytamoxifen, and its activation triggered loss of

87 st HCl transport was inhibited by tamoxifen, 4-hydroxytamoxifen, and the calmodulin antagonists, trif

88 ption was reversibly inhibited by tamoxifen, 4-hydroxytamoxifen, and trifluoperazine with IC50 values

89 treatment with antiestrogens (ICI 182,780 or 4-hydroxytamoxifen) antagonized the effects of 17beta-es

90 essary to accumulate and strip tamoxifen and 4-hydroxytamoxifen are discussed.

91 estrogen agonist (estradiol) and antagonist (4-hydroxytamoxifen) are reduced.

92 east cancer drug tamoxifen and a metabolite, 4-hydroxytamoxifen, as the target analytes.

93 oxifen resistant and were induced to grow by 4-hydroxytamoxifen, as well as other antiestrogens, as p

94 treatment with ER antagonists ICI 182,780 or 4-hydroxytamoxifen blocked resveratrol- or E(2)-induced

95 The anti-estrogen 4-hydroxytamoxifen blocks Rsk2-mediated activation of ER

96 o induced by the partial estrogen antagonist 4-hydroxytamoxifen, but not by the complete antagonist I

97 ding Raloxifene, Diethylstilbestrol, E2, and 4-hydroxytamoxifen, by employing FLuc-based optical biol

98 m osteoclasts to study effects of tamoxifen, 4-hydroxytamoxifen, calmodulin antagonists, estrogen, di

99 The median 4-hydroxytamoxifen concentrations deep in the breast wer

100 ation doubling times in estrogen-depleted or 4-hydroxytamoxifen containing medium.

101 transgenic zebrafish that express ubiquitous 4-hydroxytamoxifen-controlled Cre recombinase activity f

102 rent expression of ERbeta and treatment with 4-hydroxytamoxifen decreased tumorigenic potential of th

103 KRAB-PAX3-HBD protein and showed it to be a 4-hydroxytamoxifen-dependent transcriptional repressor o

104 ligand-binding domain of ERalpha allowed for 4-hydroxytamoxifen-dependent, synergistic activation of

105 also acquire resistance to the anti-estrogen 4-hydroxytamoxifen due to the rise of cyclin D1 levels i

106 lences activation function-1 activity in the 4-hydroxytamoxifen-ERalpha complex with the complete los

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

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

109 atment (-16 [95% CI, -22 to -9.4]) than with 4-hydroxytamoxifen gel (-1.8 [95% CI, -5.8 to 2.3]).

110 the oral tamoxifen group and minimal in the 4-hydroxytamoxifen gel group (median, 13.0 [IQR, 8.9-20.

111 I was 3.3% higher (80% CI, 2.1%-4.6%) in the 4-hydroxytamoxifen gel group compared with the oral tamo

112 40 in the oral tamoxifen group and 35 in the 4-hydroxytamoxifen gel group).

113 ous pilot studies have suggested transdermal 4-hydroxytamoxifen gel has equivalent antiproliferative

114 l trial, antiproliferative noninferiority of 4-hydroxytamoxifen gel to oral tamoxifen was not confirm

115 Noninferiority of Ki67-LI reduction by 4-hydroxytamoxifen gel was tested using analysis of cova

116 moxifen citrate, 20 mg/d, and gel placebo or 4-hydroxytamoxifen gel, 2 mg/d per breast, and oral plac

117 se cell lines, the nonsteroidal antiestrogen 4-hydroxytamoxifen has little effect on the mRNA level b

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

119 ce is presented that the estrogen antagonist 4-hydroxytamoxifen (HT) can occupy not only the core bin

120 tive bioelectrochemical interface, we detect 4-hydroxytamoxifen in human blood samples as changes in

121 of a Myc-estrogen receptor fusion protein by 4-hydroxytamoxifen in mouse cells resulted in suppressio

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

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

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

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

126 Exposure to 4-hydroxytamoxifen induced Cre-mediated recombination in

127 Similarly, the ERalpha antagonist 4-hydroxytamoxifen inhibited cofactor recruitment to the

128 reclinical studies that in JAK2V617F+ cells, 4-hydroxytamoxifen inhibits mitochondrial complex-I, act

129 with immobility at approximately 30 d after 4-hydroxytamoxifen injection.

130 4-Hydroxytamoxifen is a full agonist at a transforming g

131 ction 3, consistent with the hypothesis that 4-hydroxytamoxifen is a precursor for adduct fraction 3

132 ively minor DNA adduct of tamoxifen (dG-N(2)-4-hydroxytamoxifen) is more mutagenic than the major tam

133 nin to be induced by the synthetic estrogen, 4-hydroxytamoxifen, leading to regulated activation of a

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

135 Selection for resistance to 4-hydroxytamoxifen led to the development of the SUM44/L

136 ealed that in vitro fractions 3 and Q1 (from 4-hydroxytamoxifen) matched the major in vivo group I ad

137 prevention to investigate how tamoxifen and 4-hydroxytamoxifen may act in normal human mammary epith

138 Activating PKB with 4-hydroxytamoxifen mimicked insulin by decreasing mTOR r

139 roxytamoxifen therapeutic biosensor in which 4-hydroxytamoxifen modulates the electrical signal gener

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

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

142 factors that interact with ER complexed with 4-hydroxytamoxifen (OHT) at natural target genes in a hu

143 t findings that tamoxifen and its derivative 4-hydroxytamoxifen (OHT) can exert estrogen receptor-ind

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

145 ations of tamoxifen or its active metabolite 4-hydroxytamoxifen (OHT) induce estrogen receptor alpha

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

147 tradiol, catecholestrogens, the antiestrogen 4-hydroxytamoxifen (OHT), and dietary flavonoids.

148 We show that TAM and its active metabolite, 4-hydroxytamoxifen (OHT), can actively induce programmed

149 17beta-Estradiol (E(2)) or the antiestrogen, 4-hydroxytamoxifen (OHT), induce apoptosis in stably tra

150 alpha LBD bound to the selective antagonist 4-hydroxytamoxifen (OHT).

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

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

153 ncrease the sensitivity to hormonal therapy (4-hydroxytamoxifen) or CDK4/6 inhibitors (palbociclib).

154 ses in cAMP in response to 17beta-estradiol, 4-hydroxytamoxifen, or G-1.

155 did not show responses to 17beta-estradiol, 4-hydroxytamoxifen, or G-1.

156 minimal promoters, these regulators provide 4-hydroxytamoxifen- or RU486-inducible expression system

157 activation of exogenous AML1 (RUNX1)-ER with 4-hydroxytamoxifen prevents inhibition of G1 progression

158 was incubated with alpha-acetoxytamoxifen or 4-hydroxytamoxifen quinone methide (4-OHtamQM) to genera

159 tes of tamoxifen, alpha-acetoxytamoxifen and 4-hydroxytamoxifen quinone methide (4-OHtamQM).

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

161 In addition to obtaining 4-hydroxytamoxifen regulatable engineered proteins, thes

162 e survival of Rat-1 fibroblasts containing a 4-hydroxytamoxifen-regulated c-Myc allele, c-MycER, afte

163 not influenced by the disease-associated and 4-hydroxytamoxifen resistant ERalpha-Y537S mutant.

164 re either sensitive (parental) or resistant (4-hydroxytamoxifen-resistant (OHT(R))) to tamoxifen show

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

166 formed cells by the addition of tamoxifen or 4-hydroxytamoxifen resulted in apoptosis.

167 ressing mouse embryonic stem cells (mESC) to 4-hydroxytamoxifen, results in chromosome mis-segregatio

168 p an electrochemical algorithm to decode the 4-hydroxytamoxifen signal from glucose.

169 We also amplify the 4-hydroxytamoxifen signal using an organic electrochemic

170 To encode the 4-hydroxytamoxifen signal within glucose oxidation, we i

171 In the presence of 4-hydroxytamoxifen STAT3-ER was translocated in the nucl

172 ar models for tamoxifen resistance; that is, 4-hydroxytamoxifen-stimulated MCF7ERalphaHA cells that o

173 e data support the hypothesis that uptake of 4-hydroxytamoxifen targeted doxorubicin-formaldehyde con

174 transform the conventional glucometer into a 4-hydroxytamoxifen therapeutic biosensor in which 4-hydr

175 bited by 500 nmol/L raloxifene or 500 nmol/L 4-hydroxytamoxifen, these concentrations of antiestrogen

176 -HBD ARMS cell lines and were implanted with 4-hydroxytamoxifen timed-release pellets exhibited suppr

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

178 Systemic time-release implant delivery of 4-hydroxytamoxifen to severe combined immunodeficient mi

179 rubicin-formaldehyde conjugate targeted, via 4-hydroxytamoxifen, to the estrogen receptor (ER) and an

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

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

182 epithelial proliferative response to E2 and 4-hydroxytamoxifen was retained in the AA/-females, and

183 of a Myc-estrogen receptor fusion protein by 4-hydroxytamoxifen was sufficient to repress gas1 gene t

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

185 enzyme that adds O-GlcNAc) can be induced by 4-hydroxytamoxifen, we screened the expression of 84 HSP

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

187 ndogenous cyclin D3 mRNA upon treatment with 4-hydroxytamoxifen, which induces nuclear accumulation o

188 GFR1-amplified cell lines show resistance to 4-hydroxytamoxifen, which is reversed by small interferi

189 the separation of alpha-hydroxytamoxifen and 4-hydroxytamoxifen, which were not resolvable in methano

190 Chemical oxidation of 4-hydroxytamoxifen with silver(II) oxide, followed by in

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