ライフサイエンスコーパス: 17 beta-estradiol

1 n-3 in the rat uterus by the steroid hormone 17 beta-estradiol.

2 reduced at least ten-fold by the low dose of 17 beta-estradiol.

3 d with vehicle or with physiologic levels of 17 beta-estradiol.

4 + currents but did not occlude the effect of 17 beta-estradiol.

5 ts but was significantly less effective than 17 beta-estradiol.

6 17 beta-estradiol followed by withdrawal of 17 beta-estradiol.

7 onocytes also increased in cells deprived of 17 beta-estradiol.

8 ranscription than ER beta in the presence of 17 beta-estradiol.

9 omy and were rapidly normalized by exogenous 17-beta estradiol.

10 0 was up-regulated in the presence of 10-9 M 17-beta-estradiol.

11 xpression occurred within 2 h of exposure to 17-beta-estradiol.

12 (BK channels) are activated by tamoxifen and 17-beta-estradiol.

13 Pellets containing 17 beta-estradiol (0.25, 0.5, 1.5, and 7.5 mg released o

14 icans strains were tested in the presence of 17-beta-estradiol (10-6 M and 10-9 M) for increased grow

15 16 injections 48 h apart) or pellets (0.1 mg 17 beta-estradiol, 14 days) were not very effective in m

16 two biochemical synthetic estrogen sulfates, 17 beta-estradiol 17-sulfate (E2-17S) and 17 beta-estrad

17 17-beta estradiol (17-beta E(2)) attenuates the expressi

18 HSV-1 corneal infection model, we establish 17-beta estradiol (17-betaE) treatment of latently infec

19 odistribution and pharmacokinetic profile of 17-beta-estradiol (17-betaE) on systemic delivery using

20 icine, nocodazole, vinblastine, vincristine, 17-beta-estradiol, 2-methoxyestradiol) altered cyclooxyg

21 into four subgroups treated with either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA,

22 o four subgroups and treated with either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA,

23 th 5-alpha-dihydrotestosterone (357 mg/day), 17-beta-estradiol (23.8 microg/day), or placebo for 21 d

24 s, 17 beta-estradiol 17-sulfate (E2-17S) and 17 beta-estradiol 3,17-disulfate (E2-3,17S).

25 fate (E1-3S), estriol 3-sulfate (E3-3S), and 17 beta-estradiol 3-sulfate (E2-3S), and two biochemical

26 mmediately after a subcutaneous injection of 17-beta-estradiol 3-benzoate (EB; 5 mug/0.1 mL) or 24 h

27 nistration of a single physiological dose of 17 beta-estradiol (40 microg/kg) to ovariectomized immat

28 ls capable of limited self-renewal, and that 17 beta-estradiol acts in vivo and in vitro to attenuate

29 reversal of the modulation, suggesting that 17 beta-estradiol acts via G-protein activation.

30 several substrates, including testosterone, 17 beta-estradiol, amitriptyline, and most notably aflat

31 These data suggest that 17 beta-estradiol and anabasine reduce chronic bladder i

32 Both 17 beta-estradiol and estrone improved retention on an e

33 ts of administration into the hippocampus of 17 beta-estradiol and estrone on retention of T-maze foo

34 The steroid hormones 17 beta-estradiol and progesterone play a central role i

35 In addition, treatment of mice with 17 beta-estradiol and progesterone results in the rapid

36 ation of a common tumor-derived AR allele by 17 beta-estradiol and progesterone was inhibited through

37 The complementary treatment of 17 beta-estradiol and the nicotinic agonist anabasine re

38 intraperitoneally with vehicle or 0.2 mg/kg 17 beta-estradiol and then were re-tested 24 and 48 h la

39 bone loss, was suppressed in osteoclasts by 17-beta estradiol and NAC.

40 nt acridine orange uptake, was unaffected by 17-beta-estradiol and diethylstilbestrol at concentratio

41 OVX animals had decreased serum levels of 17-beta-estradiol and increased serum levels of osteocal

42 Female BALB/c mice were treated with 17-beta-estradiol and inoculated intravaginally with wil

43 Both RBCK1 and FKBPL are upregulated by 17-beta-estradiol and interact within heat shock protein

44 ripheral blood macrophages in the absence of 17 beta-estradiol, and the observed increase in message

45 otective effects of testosterone propionate, 17-beta estradiol, and dihydrotestosterone on FMNs of P7

46 iocyanate as major endogenous substrates and 17 beta-estradiol as a novel minor endogenous substrate

47 CVCs were treated with 17 beta-estradiol at concentrations of 0, 5, and 10 nmol

48 5) received daily injections of 10 microg of 17 beta-estradiol benzoate (EB), or 250 microg of testos

49 utive treatment cycles with vehicle (Oil) or 17-beta-estradiol benzoate (E).

50 hed after ovariectomy, and administration of 17-beta-estradiol benzoate (EB) restored this escalated

51 mpounds were 8- to 114-fold more potent than 17 beta-estradiol (betaE2), but lacked ER binding capaci

52 125I-17 beta-estradiol binding studies showed the presence of

53 nus of alpha4 prevented AChR potentiation by 17-beta-estradiol by disruption of its binding site.

54 uggest that at physiological concentrations, 17 beta-estradiol can have immediate actions on neostria

55 rtic rings treated with NG-nitro-L-arginine, 17 beta-estradiol caused dose-dependent (0.3 to 30 mumol

56 tiation, were enhanced in cells treated with 17 beta-estradiol compared with control cells.

57 Here we show that the ER agonist 17 beta-estradiol completely abolished IL-6-inducible MM

58 17 beta-Estradiol conjugated to bovine serum albumin als

59 17 beta-Estradiol did not affect the kinetics (i.e., aff

60 s that decreased concentrations of estrogen (17 beta-estradiol) directly cause an increase in CD16 ex

61 In this study, we demonstrate that 17 beta-estradiol (E(2)) treatment of hippocampal neuron

62 (DHTP, a non-aromatizable form of androgen), 17 beta-estradiol (E), or placebo.

63 ssed the effect of 2 weeks of treatment with 17 beta-estradiol (E, 100 micrograms.kg-1.d-1, n = 12) o

64 Estrogens such as 17-beta estradiol (E(2)) play a critical role in sporadi

65 th either a subcutaneous sham implant (OVX), 17-beta estradiol (E) implant (OVX+E) or E implant plus

66 We report here that 17-beta-estradiol (E(2)) causes a 3- to 5-fold increase

67 17-beta-estradiol (E(2)) substantially blocks ATR activi

68 In estrogen-receptor positive cells, 17-beta-estradiol (E(2)) transcriptionally stimulated PC

69 G(1)/S transition induced in MCF-7 cells by 17-beta-estradiol (E(2)) with associated inhibition of b

70 tudies from our laboratory have demonstrated 17 beta estradiol (E2) induction of p53 protein expressi

71 group for 3 days with vehicle, another with 17 beta estradiol (E2), and a third with tamoxifen.

72 A single dose of 17 beta-estradiol (E2) (100 microgram/kg) was injected s

73 ious work from our laboratory has shown that 17 beta-estradiol (E2) administration to prepubertal fem

74 te the possibility of an interaction between 17 beta-estradiol (E2) and glutathione in protecting cel

75 tumor growth, we studied VEGF regulation by 17 beta-estradiol (E2) and tamoxifen, two agents that ca

76 17 beta-estradiol (E2) enhanced the inhibitory effect of

77 The 4-hydroxy metabolite of 17 beta-estradiol (E2) has been implicated in the carcin

78 Gender influences mediated by 17 beta-estradiol (E2) have been associated with suscept

79 sr1) is crucial for the protective effect of 17 beta-estradiol (E2) in murine experimental autoimmune

80 Previously, we found that 17 beta-estradiol (E2) increased the number of arcuate n

81 under which physiological concentrations of 17 beta-estradiol (E2) inhibit oxidative modification of

82 iously established the protective effects of 17 beta-estradiol (E2) on experimental autoimmune enceph

83 e subcutaneously implanted with time-release 17 beta-estradiol (E2) pellets from 30 to 90 days, the p

84 Exposure to 0.1 pM, 10 pM, and 1 nM 17 beta-estradiol (E2) resulted in monotonic inhibition

85 CYP1B1) catalyze the oxidative metabolism of 17 beta-estradiol (E2) to catechol estrogens (2-OHE2 and

86 We have demonstrated previously that 17 beta-estradiol (E2) treatment of BALB/c mice transgen

87 17 beta-estradiol (E2) treatment produced strong protect

88 Serum testosterone (T), 17 beta-estradiol (E2), and dihydrotestosterone (DHT), a

89 ariectomized (OVX) and implanted with either 17 beta-estradiol (E2), progesterone (P4) or received an

90 rosine kinases that are activated in vivo by 17 beta-estradiol (E2), uteri from ovariectomized mice w

91 ocampal NMDA receptors and PKA activation in 17 beta-estradiol (E2)-induced enhancement of object mem

92 ceptors, is widely expressed in a variety of 17 beta-estradiol (E2)-responsive reproductive tissues a

93 adal hormone-free medium and pretreated with 17 beta-estradiol (E2).

94 cal immunosensors for sensitive detection of 17-beta estradiol (E2) and ethinylestradiol (EE2) are de

95 er susceptibility gene, BRCA1, is induced by 17-beta estradiol (E2) in estrogen receptor containing b

96 The inaccuracy of 17-beta estradiol (E2) measurements affects its use as a

97 e, we studied the effects of the sex hormone 17-beta estradiol (E2) on growth, oxidative stress, and

98 It is known that 17-beta estradiol (E2) regulates adipose tissue function

99 l conjugated equine estrogen (CEE), (2) oral 17-beta estradiol (E2), and (3) subcutaneously implanted

100 implicated female sex hormones, particularly 17-beta estradiol (E2), in the pathogenesis of these dis

101 17-beta-estradiol (E2) acting via estrogen receptors inh

102 Here, we studied how 17-beta-estradiol (E2) and IGF-1 affect ER transcription

103 xposed to physiologically relevant levels of 17-beta-estradiol (E2) and progesterone (P4).

104 ies have demonstrated a relationship between 17-beta-estradiol (E2) deficiencies and skeletal bone lo

105 17-beta-estradiol (E2) enhanced responsiveness of BMSCs

106 Hormones such as 17-beta-estradiol (E2) have been implicated in cerebella

107 ndogenous progesterone receptor (PR) gene by 17-beta-estradiol (E2) in cells stably transfected with

108 in the adult suggesting an important role of 17-beta-estradiol (E2) in this brain structure.

109 into the adipocyte lineage was suppressed by 17-beta-estradiol (E2) in WT female mice but not in NOER

110 17-beta-Estradiol (E2) is a steroid hormone involved in

111 17-Beta-estradiol (E2) is a steroid hormone involved in

112 that 11-ketotestosterone (11 kT) raised and 17-beta-estradiol (E2) lowered the EOD frequency of inta

113 Here we examined the effect of 17-beta-estradiol (E2) on the maturational response trig

114 We show in this study that 17-beta-estradiol (E2) promotes the differentiation of f

115 Our laboratory recently demonstrated that 17-beta-estradiol (E2) promotes the GM-CSF-mediated deve

116 f IRS-1 was translocated to the nucleus upon 17-beta-estradiol (E2) treatment; (2) E2-dependent nucle

117 In breast cancer cells, 17-beta-estradiol (E2) upregulates the expression of ins

118 ls from MOER and wild type mice responded to 17-beta-estradiol (E2) with comparable activation of ERK

119 ucocorticoids in the inhibition of estrogen (17-beta-estradiol (E2))-regulated estrogen receptor (ER)

120 Estrogens, most commonly 17-beta-estradiol (E2), can suppress apoptosis in MCF-7

121 ere examined after treatment with ER agonist 17-beta-estradiol (E2), the pure ER antagonist ICI 182,7

122 We previously reported that 17-beta-estradiol (E2)-induced mitochondrial reactive ox

123 this study was to investigate the effects of 17-beta-estradiol (E2)-induced reactive oxygen species (

124 ation of prolactin (PRL) expression in TG by 17-beta-estradiol (E2).

125 We demonstrate that estrogen (17-beta-estradiol, E2) is capable of augmenting FoxP3 ex

126 ose that physiological levels of circulating 17 beta-estradiol elevate basal NO release from the endo

127 ted environmental concentrations resulted in 17-beta-estradiol equivalency quotients ranging from 0.0

128 mazepine), and steroidal estrogens (estrone, 17-beta-estradiol, estriol, and 17-alpha-ethinylestradio

129 n culture models of DC differentiation, that 17-beta-estradiol exerts opposing effects on differentia

130 0(-8)M) of 17 beta-estradiol, or 1 x 10(-8)M 17 beta-estradiol followed by withdrawal of 17 beta-estr

131 Treatment with 17 beta-estradiol for 6 months and a 10-day course of me

132 ouse and human hepatocytes were treated with 17-beta-estradiol for 24 h.

133 plants possesses structural similarity with 17 beta-estradiol found in mammals.

134 nd that substrates such as leukotriene D(4), 17-beta-estradiol glucuronide, and the leukotriene inhib

135 0.05 mg 17 beta-estradiol (low E2), or 5 mg 17 beta-estradiol (high E2) before i.p. injection of tal

136 to modulate transcription in the presence of 17 beta-estradiol, ICI 182,780, tamoxifen, raloxifene, g

137 ERalpha mediates the effects of 17-beta-estradiol in both males and females, and was the

138 ated in primary neuronal cultures exposed to 17-beta-estradiol in vitro, further confirming the direc

139 The 17-beta estradiol increased glutathione and glutathione

140 animals had a progressive decrease in serum 17-beta-estradiol, increased serum osteocalcin and IL-6,

141 17-beta estradiol increases c-rasH MCF-7 growth but abol

142 At concentrations of 10(-8) to 10(-7) M, 17-beta-estradiol induced up to a 5-fold increase of bot

143 17 beta-Estradiol-induced relaxation of rat aortic rings

144 eptor antagonist ICI 164384 had no effect on 17 beta-estradiol-induced relaxations.

145 inhibition of entry of extracellular Ca2+ in 17 beta-estradiol-induced vasorelaxation in depolarized

146 17 beta-Estradiol induces vasodilation in vitro and in v

147 The RIDE system makes use of the 17-beta estradiol-inducible promoter system linked to in

148 footshock paradigm to test whether a dose of 17 beta-estradiol ineffective as a single injection (sub

149 In rat aortic rings, 17 beta-estradiol inhibited the increase of 45Ca uptake

150 2-Methoxyestradiol (2ME(2)), a metabolite of 17-beta-estradiol, inhibits angiogenesis and has additio

151 While 17 beta-estradiol is normally present at high concentrat

152 ainment of physiological (for females) serum 17 beta-estradiol levels.

153 can be accounted for by differences in serum 17 beta-estradiol levels.

154 nted for by MPA-induced alterations in serum 17 beta-estradiol levels.

155 e effects of estrogen without altering serum 17 beta-estradiol levels.

156 -release pellets containing placebo, 0.05 mg 17 beta-estradiol (low E2), or 5 mg 17 beta-estradiol (h

157 d-type and estrogen receptor-deficient mice, 17 beta-estradiol markedly inhibited to the same degree

158 Because tamoxifen and 17-beta-estradiol may share a common binding site, we hy

159 Furthermore, a previous study indicated that 17-beta-estradiol might bind an extracellular site on th

160 h either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA, or (4) vehicle and were subject

161 h either (1) 17 beta-estradiol, (2) MPA, (3) 17 beta-estradiol + MPA, or (4) vehicle, and balloon inj

162 The maximum reduction by 17 beta-estradiol occurred at picomolar concentrations.

163 -specific biochemical markers; the effect of 17 beta-estradiol on CFU-OB self-renewal is absent in mi

164 for estrogen receptors and for the effect of 17 beta-estradiol on formation of calcified nodules, cal

165 compared the effects of 2 delivery routes of 17 beta-estradiol on spatial learning and dendritic spin

166 We therefore investigated the influence of 17-beta-estradiol on the production, localization, and f

167 us administration of either low or high dose 17 beta-estradiol or tibolone did not alter infarct volu

168 17-beta-Estradiol or estrogen receptor beta agonists dip

169 breast cancer cell line (MCF-7) treated with 17-beta-estradiol or vehicle control were used to develo

170 tradiol, physiologic levels (1 x 10(-8)M) of 17 beta-estradiol, or 1 x 10(-8)M 17 beta-estradiol foll

171 sterone, but not 5 beta-dihydrotestosterone, 17 beta-estradiol, or medroxyprogesterone acetate, also

172 plemented with testosterone propionate, with 17-beta-estradiol, or with 5-alpha-dihydrotestosterone.

173 phs were made at 4-month intervals and serum 17-beta-estradiol, osteocalcin, and interleukin (IL)-6,

174 ed pellets designed to release 1.5 or 5.0 mg 17 beta-estradiol over 30 days.

175 Hormone replacement with subdermal 17-beta-estradiol pellets releasing either 6, 14, or 28

176 yte-derived macrophages were treated with no 17 beta-estradiol, physiologic levels (1 x 10(-8)M) of 1

177 Under the perforated patch configuration, 17 beta-estradiol potentiated kainate-induced currents i

178 J, DBA/2J, AKR/J, BALB/cJ) supplemented with 17-beta-estradiol presented the opposite effect, a reduc

179 17 beta-Estradiol primarily targeted L-type currents, an

180 A rise in 17-beta estradiol production associated with ART increas

181 17 beta-Estradiol promoted apoptosis of murine osteoclas

182 These results suggest that 17 beta-estradiol promotes osteoblastic differentiation

183 ary, in the apolipoprotein E-deficient mouse 17-beta-estradiol protects against atherosclerotic lesio

184 ly, these data show that the steroid hormone 17 beta-estradiol, regulates transcription of the syndec

185 microarray dose-response study, to identify 17 beta-estradiol sensitive genes in breast cancer cells

186 We showed that 17-beta estradiol significantly reduces the overall cyto

187 We discovered that 17-beta estradiol supplementation of ovariectomized mice

188 In addition, 17-beta-estradiol-supplemented castrated mice showed a h

189 were exposed to testosterone propionate and 17-beta-estradiol (T + E2), the tissue recombinants resp

190 ibroblast mitogenic activity is unaltered by 17-beta estradiol/tamoxifen pretreatment in vitro.

191 ogic concentrations (1 nmol/liter) of either 17-beta-estradiol, testosterone or progesterone before p

192 sules filled with oil (vehicle) or a dose of 17 beta-estradiol that produces physiological hormone le

193 Within 48 hours of injection of 17-beta-estradiol, the number of perirhinal neurons doub

194 tion, and as a ternary complex with NADH and 17 beta-estradiol to 1.7 A resolution.

195 Female BALB/c mice were treated with 17-beta estradiol to promote susceptibility to N. gonorr

196 urther increased after the administration of 17-beta-estradiol to castrated B6 male mice as compared

197 Topical treatments with 17-beta-estradiol to the clipped dorsal skin of mice arr

198 Cytokine release from 17 beta-estradiol-treated or untreated monocytes was the

199 acity to colonize the lower genital tract of 17-beta estradiol-treated female BALB/c mice during comp

200 17-beta-Estradiol-treated epidermis demonstrated a simil

201 Twenty-one days of 17 beta-estradiol treatment resulted in a significantly

202 Importantly, although 17 beta-estradiol treatment resulted in decreased collag

203 esponse curves show that the potentiation by 17 beta-estradiol was evident at a concentration as low

204 Using whole-cell patch-clamp techniques, 17 beta-estradiol was found to reduce Ba2+ entry reversi

205 The potentiation by 17 beta-estradiol was similar to the enhancement of kain

206 potentiation of kainate-induced currents by 17-beta-estradiol was likely a G-protein(s) coupled, cAM

207 The serum concentrations of testosterone and 17 beta-estradiol were 2.53 ng/ml and 201 pg/ml in OVX +

208 educe Ba2+ currents with similar efficacy to 17 beta-estradiol, whereas estrone and 2-methoxyestriol

209 by circulating levels of the steroid hormone 17-beta-estradiol, which is predominantly synthesized by

210 es preceded a significant reduction in serum 17-beta-estradiol, which occurred between 4 and 8 months