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• W2063553703 abstract "The relationship between nuclear binding of the receptor-estrogen complex (R-E) and estrogenic responses was examined. Nuclear-bound R-E was measured by the [3H] estradiol exchange assay, which permits the quantification of R-E as a function of either endogenous or non labeled estrogen. The quantity of nuclear R-E fluctuated as a function of blood levels of estrogen during the estrous cycle in the rat. This indicates that the accumulation of the R-E complex by the nucleus of uterine cells may be of physiologic significance and under the control of endogenous estrogen.This is a review of estrogen receptors, largely taken from the authors' works, including estrogen receptors in the rat estrous cycle, in response to exogenous estrogens, endogenous estrogens, early responses, and the action of antiestrogens. Their method of measuring nuclear estrogen-receptor complexes entails incubating nuclear fractions with labeled estradiol, and with labeled estradiol in an excess of diethylstilbestrol, and quantitating the difference. Specific nuclear binding was documented in uterus, vagina, and pituitary of rats, in response to estradiol, diethylstilbestrol, estrone, and estriol, with a maximum of binding sites in proestrus, and the peak of estrogen secretion. The amount of estradiol bound increased with estradiol dose, but the rate of disappearance of bound nuclear estrogens was also more rapid with estrogen dose. Estradiol and estriol exhibited equal influences on early events such as RNA synthesis, but estriol did not maintain nuclear estrogen complex after 3 hours, nor permanent increase in uterine dry weight. These data lead the authors to suggest that a certain level of nuclear-receptor must be retained for at least 6 hours, as opposed to the theory that pivotal events like increased uterine blood flow, fluid imbibition, glucose transport, histamine release, and synthesis of the IP protein, is all that is required for uterine growth. Using the estrogen antagonists nafoxidine (Upjohn, 11,100 A), Cl-628, and clomiphene, and the charcoaldextran assay of total cytoplasmic estrogen-receptor binding, it was shown that the antagonists do stimulate nuclear binding, for up to 19 days in rats, but inhibit synthesis or replenishment of cytoplasmic receptors. Thus, the often observed fact that these estrogen antagonists are not antagonistic at 24 hours, but do antagonize estradiol later, is explained by prolonged retention of nuclear receptors." @default.
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• W2063553703 date "1976-03-01" @default.
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• W2063553703 title "Estrogen‐receptor binding: Relationship to estrogen‐induced responses" @default.
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• W2063553703 doi "https://doi.org/10.1080/15287397609529359" @default.
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