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 l and decreased the antagonist activity of 4-hydroxytamoxifen.

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

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

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

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

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

9 estrogen receptor domain are treated with 4-hydroxytamoxifen.

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

11 e estrogen receptor that selectively binds 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 n receptor-positive breast cancer cells to 4-hydroxytamoxifen.

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

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

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

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

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

22 mpletely dependent on ectopic provision of 4-hydroxytamoxifen.

23 splicing activities that highly depend on 4-hydroxytamoxifen.

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

25 adiol and increased antagonist activity of 4-hydroxytamoxifen.

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

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

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

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

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

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

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

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

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

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

36 rx1creER-egfp;td-Tomato mice and delivered 4-hydroxytamoxifen (4-OHT) to the mouse calvaria, subperio

37 rylic acid (GW7604) as a derivative of (Z)-4-hydroxytamoxifen (4-OHT) was linked by diaminoalkane spa

38 4-Hydroxytamoxifen (4-OHT), a selective estrogen receptor

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

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

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

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

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

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

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

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

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

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

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

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

51 bles cell proliferation in the presence of 4-hydroxytamoxifen (4-OHT).

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

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

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

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

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

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

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

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

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

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

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

63 gen receptor modulators (SERMs), including 4-hydroxytamoxifen (4OHT), activate AF-1 preferentially ra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 4-Hydroxytamoxifen and alpha-hydroxytamoxifen appear to be

80 thylene bisphenol (BPTPE), and antagonists 4-hydroxytamoxifen and endoxifen.

81 of HNRNPA2/B1 reduced MCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant, suggesting a role for

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

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

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

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

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

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

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

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

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

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

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

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

94 4-Hydroxytamoxifen and alpha-hydroxytamoxifen appear to be the proximate metabolites

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

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

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

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

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

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

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

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

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

104 The median 4-hydroxytamoxifen concentrations deep in the breast were

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

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

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

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

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

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

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

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

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

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

115 he oral tamoxifen group and minimal in the 4-hydroxytamoxifen gel group (median, 13.0 [IQR, 8.9-20.6]

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

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

118 s pilot studies have suggested transdermal 4-hydroxytamoxifen gel has equivalent antiproliferative ef

119 trial, antiproliferative noninferiority of 4-hydroxytamoxifen gel to oral tamoxifen was not confirmed

120 Noninferiority of Ki67-LI reduction by 4-hydroxytamoxifen gel was tested using analysis of covari

121 xifen citrate, 20 mg/d, and gel placebo or 4-hydroxytamoxifen gel, 2 mg/d per breast, and oral placeb

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

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

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

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

126 ve bioelectrochemical interface, we detect 4-hydroxytamoxifen in human blood samples as changes in th

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

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

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

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

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

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

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

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

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

136 clinical studies that in JAK2V617F+ cells, 4-hydroxytamoxifen inhibits mitochondrial complex-I, activ

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

138 4-Hydroxytamoxifen is a full agonist at a transforming gro

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

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

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

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

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

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

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

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

147 xytamoxifen therapeutic biosensor in which 4-hydroxytamoxifen modulates the electrical signal generat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 s in cAMP in response to 17beta-estradiol, 4-hydroxytamoxifen, or G-1.

163 id not show responses to 17beta-estradiol, 4-hydroxytamoxifen, or G-1.

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

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

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

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

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

169 In addition to obtaining 4-hydroxytamoxifen regulatable engineered proteins, these

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

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

172 t influenced by the disease-associated and 4-hydroxytamoxifen resistant ERalpha-Y537S mutant.

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

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

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

176 ssing mouse embryonic stem cells (mESC) to 4-hydroxytamoxifen, results in chromosome mis-segregation

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

178 We also amplify the 4-hydroxytamoxifen signal using an organic electrochemical

179 To encode the 4-hydroxytamoxifen signal within glucose oxidation, we int

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

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

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

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

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

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

186 ansform the conventional glucometer into a 4-hydroxytamoxifen therapeutic biosensor in which 4-hydrox

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 96, and the partial agonist-antagonist trans-hydroxytamoxifen) with those that are predicted to conta

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