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

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

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

5 ine estrogen receptor that selectively binds 4-hydroxytamoxifen.

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

7 nctional unless associated with tamoxifen or 4-hydroxytamoxifen.

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

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

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

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

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

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

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

15 completely dependent on ectopic provision of 4-hydroxytamoxifen.

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

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

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

19 tradiol and increased antagonist activity of 4-hydroxytamoxifen.

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

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

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

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

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

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

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

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

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

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

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

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

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

33 4-Hydroxytamoxifen (4-OHT), a selective estrogen recepto

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 4-Hydroxytamoxifen and alpha-hydroxytamoxifen appear to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 4-Hydroxytamoxifen is a full agonist at a transforming g

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 17beta-Estradiol (E(2)) or the antiestrogen, 4-hydroxytamoxifen (OHT), induce apoptosis in stably tra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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