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1 sms other than the action of tamoxifen as an estrogen antagonist.
2 3G), and could be inhibited by tamoxifen, an estrogen antagonist.
3 iated by estrogen, estrogen deprivation, and estrogen antagonists.
4 reporter gene, and was inhibited by specific estrogen antagonists.
5 r in the presence of estrogen metabolites or estrogen antagonists.
6 ity, the antiestrogens then function as pure estrogen antagonists.
8 sphorylation was also induced by the partial estrogen antagonist 4-hydroxytamoxifen, but not by the c
9 hanges were also observed in the presence of estrogen antagonist and were corroborated in the estroge
10 Brg1/Brm node is a major cellular target for estrogen antagonists, and thereby also implicate prohibi
14 tin structural changes could be repressed by estrogen antagonist ICI 182 780 in MCF-7 cells yet were
18 activation and reversed the activity of the estrogen antagonists ICI182780 (ICI) and tamoxifen (TAM)
19 characteristic feature of AF2ER is that the estrogen antagonists ICI182780 and tamoxifen (TAM) act a
20 ved in U2OS cells, SP500263 acts as a strong estrogen antagonist in an MCF-7 breast cancer proliferat
22 n receptor modulator (SERM) that is a potent estrogen antagonist in mammary and uterine tissue while
25 with male slices or exposed to estrogen, and estrogen antagonists inhibited song circuit development
26 hromatin modifiers Brg1/Brm are required for estrogen antagonist-mediated growth suppression through
28 ulted in a substantial (10-fold) increase in estrogen antagonist potency relative to raloxifene in an
29 ues and serum lipids while displaying potent estrogen antagonist properties in the breast and uterus.
30 triarylethylenes to improve ER affinity and estrogen antagonist properties, were prepared with the u
31 nditional knockout pups with fulvestrant, an estrogen antagonist, reestablished the balance between t
32 naling was prevented and even potentiated by estrogen antagonists such as tamoxifen, suggesting that
33 naling was prevented and even potentiated by estrogen antagonists such as tamoxifen, suggesting that
35 d controls, whereas females administered the estrogen antagonist tamoxifen prior to stress were not i
36 he absence of estrogen or in the presence of estrogen antagonists tamoxifen or ICI 182780; second, am
37 ependent cellular inhibitory responses to an estrogen antagonist, tamoxifen (TAM), via at least in pa
38 gulatory gene NAP1L1, an adhesin MAGE-D2, an estrogen-antagonist, the metastasis marker MTA1, the apo
40 dditive impact on cell growth, whereas known estrogen antagonists were found to neutralize agonist ef
41 ct of BPA was blocked by Fulvestrant, a full estrogen antagonist, while the effect of estradiol was n