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1 rylation in RAW264.7 cells relative to other estrogen agonists.
2 hormone replacement therapy and other novel estrogen agonists.
3 e enhanced GR degradation in the presence of estrogen agonists.
4 ifen, LY117018, and LY317783) did not act as estrogen agonists.
5 Our results demonstrate that treatment with estrogen agonists (17beta-estradiol [E2], diethylstilbes
6 n together with our published reports of the estrogen agonist activities of DIM, the present results
7 ities due to its ERbeta selectivity, partial estrogen agonist activity, and non-enzymatic conversion
8 enbolone, for the nonsteroidal semisynthetic estrogen agonist, alpha-zearalanol, and the synthetic pr
9 igands which, like tamoxifen (1), can elicit estrogen agonist and antagonist effects, in turn, in non
11 e substances in the soybean that demonstrate estrogen agonist and/or antagonist effects when they bin
12 esent study, we characterized the effects of estrogen agonists and antagonists (anti-estrogens [AE])
13 recognition of several structurally diverse estrogen agonists and antagonists (the synthetic nonster
14 vidence suggests that soy isoflavones act as estrogen agonists and have beneficial skeletal effects,
15 the absence of E2, resveratrol exerts mixed estrogen agonist/antagonist activities in some mammary c
17 estrogen receptor (ER) modulator, is a mixed estrogen agonist/antagonist that has been shown to preve
19 selective estrogen receptor modulator (mixed estrogen agonist/antagonist) with potential psychoprotec
20 er, these results demonstrate that the mixed estrogen agonist/antagonist, raloxifene, induces apoptos
22 t that the addition of a fluorescein-labeled estrogen agonist displaces a SNAPFL-labeled antiestrogen
23 crease in GR protein levels, suggesting that estrogen agonists down regulate the GR via the proteasom
25 ast, isoflavone treatment had no significant estrogen agonist effects and minimal antagonistic effect
27 bsence of hormone while their affinities for estrogen agonist (estradiol) and antagonist (4-hydroxyta
30 antagonistic activities, as combinations of estrogen agonists had an additive impact on cell growth,
34 heir ability to function as tissue-selective estrogen agonists in vivo has been assayed in a short-te
36 d that diethylstilbestrol (DES), a synthetic estrogen agonist, inhibits thrombin-induced Ca(2+) influ
38 gen receptor modulators (SERMs) that possess estrogen agonist-like actions on bone tissues and serum
40 se elements may explain the tissue-selective estrogen agonist or antagonist activity of compounds suc
41 eceptors (ER) and may variably act as either estrogen agonists or antagonists depending on the estrog
44 ion of the ERalpha AF1 region in response to estrogen (agonist), tamoxifen (antagonist), and growth f
45 ammary and uterine tissue while acting as an estrogen agonist to maintain bone density and lower seru
46 n diet, was reported recently to serve as an estrogen agonist with cultured MCF-7 cells transfected w
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