![Percent inhibition of 1 nM [3H]estradiol binding by co-incubation with 100 nM of different competitor ligands for 1 hour at 37°C (human body temperature) in cultured human aortic smooth muscle cells (SMCs) in vitro. The competitor ligands included the estrogens estradiol (E2), estrone (E1), estriol (E3), 17α-estradiol (17α-E2; alfatradiol); the antiestrogen fulvestrant (Fulv; ICI-182,780); and the estrogen esters estradiol valerate (EV), estradiol cypionate (EC), estradiol benzoate (EB), and estrone sulfate (E1S). The cells were found to express both ERα and ERβ. The shown results relate to estrogen receptor binding affinity (with 50% inhibition of binding corresponding to the half-maximal inhibitory concentration or IC50). Source of the values: (April 2000). "Clinically used estrogens differentially inhibit human aortic smooth muscle cell growth and mitogen-activated protein kinase activity". Arterioscler. Thromb. Vasc. Biol. 20 (4): 964–72. DOI:10.1161/01.atv.20.4.964. PMID 10764660.](http://upload.wikimedia.org/wikipedia/commons/8/89/Inhibition_of_estradiol_binding_by_selected_estrogens%2C_antiestrogens%2C_and_estrogen_esters_to_human_aortic_tissue_in_vitro.png)
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Summary
| Description |
Percent inhibition of 1 nM [3H]estradiol binding by co-incubation with 100 nM of different competitor ligands for 1 hour at 37°C (human body temperature) in cultured human aortic smooth muscle cells (SMCs) in vitro. The competitor ligands included the estrogens estradiol (E2), estrone (E1), estriol (E3), 17α-estradiol (17α-E2; alfatradiol); the antiestrogen fulvestrant (Fulv; ICI-182,780); and the estrogen esters estradiol valerate (EV), estradiol cypionate (EC), estradiol benzoate (EB), and estrone sulfate (E1S). The cells were found to express both ERα and ERβ. The shown results relate to estrogen receptor binding affinity (with 50% inhibition of binding corresponding to the half-maximal inhibitory concentration or IC50).
Source of the values:
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| Source | Own work |
| Author | Medgirl131 |
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