ライフサイエンスコーパス: estrogen agonist

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

10 tor (ER) ligands capable of tissue selective estrogen agonist and antagonist effects.

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

16 xifen have demonstrated such tissue-specific estrogen agonist/antagonist effects.

17 estrogen receptor (ER) modulator, is a mixed estrogen agonist/antagonist that has been shown to preve

18 Tamoxifen is a mixed estrogen agonist/antagonist with as yet unexplored effec

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

21 Raloxifene, a mixed estrogen agonist/antagonist, was developed to prevent os

22 logy of E(4) and BMI-135 as less-potent full-estrogen agonists as well as their molecular mechanisms

23 t that the addition of a fluorescein-labeled estrogen agonist displaces a SNAPFL-labeled antiestrogen

24 crease in GR protein levels, suggesting that estrogen agonists down regulate the GR via the proteasom

25 tivity is compromised because treatment with estrogen agonists down regulates GR protein levels.

26 ast, isoflavone treatment had no significant estrogen agonist effects and minimal antagonistic effect

27 f tamoxifen is ascribed to its genotoxic and estrogen agonist effects.

28 bsence of hormone while their affinities for estrogen agonist (estradiol) and antagonist (4-hydroxyta

29 Relative to a full estrogen agonist (ethynyl estradiol) and the SERM raloxi

30 2-b:4,5-b':7,8-b'']triindole (CTr), a potent estrogen agonist from food plants.

31 antagonistic activities, as combinations of estrogen agonists had an additive impact on cell growth,

32 In contrast, SP500263 acts as a strong estrogen agonist in a strictly ER-alpha-specific manner

33 strogen antagonist in human breast but as an estrogen agonist in the uterus.

34 In summary, genistein can act as an estrogen agonist in vivo and in vitro, resulting in the

35 heir ability to function as tissue-selective estrogen agonists in vivo has been assayed in a short-te

36 Furthermore, estrogen agonists inhibit glucocorticoid induction of p2

37 d that diethylstilbestrol (DES), a synthetic estrogen agonist, inhibits thrombin-induced Ca(2+) influ

38 A dietary source of a partial estrogen agonist is the plant-based group of phytoestrog

39 gen receptor modulators (SERMs) that possess estrogen agonist-like actions on bone tissues and serum

40 Selective estrogen agonists may be superior to conventional estrog

41 se elements may explain the tissue-selective estrogen agonist or antagonist activity of compounds suc

42 eceptors (ER) and may variably act as either estrogen agonists or antagonists depending on the estrog

43 TMBPF did not show estrogen-agonist or antagonist activity in the estrogen

44 However, no estrogen agonist reduced RANKL stimulation of osteoclast

45 ion of the ERalpha AF1 region in response to estrogen (agonist), tamoxifen (antagonist), and growth f

46 ammary and uterine tissue while acting as an estrogen agonist to maintain bone density and lower seru

47 n diet, was reported recently to serve as an estrogen agonist with cultured MCF-7 cells transfected w