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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen (E) induction of riboflavin carrier protein (RCP) in the chicken oviduct and liver was investigated to compare and contrast the kinetics, hormonal specificity and modulation of its elaboration in the 2 steroid-responsive tissues. During primary stimulation, continued daily E administration to immature female chicks elicited, after an initial lag, rapid growth and RCP content of the overduct; neither progesterone (P) nor testosterone (T) could substitute for E in this respect. Furthermore, P given along with E curtailed tissue growth and its RCP content, whereas E + T had a synergistic effect on tissue growth only. During secondary stimulation, E administration steeply enhanced both tissue weight and RCP content without any lag. Interestingly, P (but not T) could substitute for E in augmenting magnum RCP concentration to a comparable extent while a concomitant effect on tissue growth was less marked. In contrast, hepatic induction of RCP was absolutely E-specific during both primary and secondary stimulations. Secondary stimulation with either E or P of E-primed birds enhanced the rates of RCP synthesis in the oviduct relative to that of total protein, whereas in the liver only E was effective in this regard. The absolute rate of E-induced RCP synthesis in both the steroid-stimulated tissues was significantly higher than that of general protein elaboration.
Mol Cell Endocrinol 1986 Mar
PMID:Hormonal induction of riboflavin carrier protein in the chicken oviduct and liver: a comparison of kinetics and modulation. 395 57

Ovariectomy or ovariohysterectomy on day 18 of pregnancy augmented mammary beta-casein content 28 h later. Progesterone injected immediately and 12 h after ovariectomy showed a clear inhibitory effect on casein synthesis. Estrogen induced a significant increase in mammary beta-casein content when injected 12 h after surgery. Treatment with CB-154 to prevent prolactin release did not affect the increase of casein induced by ovariectomy. When CB-154 was injected to ovariohysterectomized pregnant rats, significant reduction of casein synthesis was obtained. According to these findings, rat placental lactogen in the absence of prolactin and progesterone induces beta-casein synthesis. Therefore prolactin, ovarian and placental hormones interplay at the end of pregnancy for full expression of the mammary gland genome.
Mol Cell Endocrinol 1985 Feb
PMID:Hormonal regulation of casein synthesis at the end of pregnancy. 397 61

The relative induction of FSH and LH receptors in the granulosa cells of immature rat ovary by pregnant mare serum gonadotropin (PMSG) has been studied. A single injection of PMSG (15 IU) brought about a 3- and 12-fold increase in FSH and LH receptor concentration, respectively, in the granulosa cells. Maximal concentration was reached by 72 h but the receptor levels showed a sharp decline during the next 24-48 h. The kinetic properties of the newly formed FSH receptors were indistinguishable from the pre-existing ones. The induced FSH receptors were functional as demonstrated by an increase in the in vitro responsiveness of the cells to exogenous FSH in terms of progesterone production. Treatment of immature rats with cyanoketone, an inhibitor of delta 5,3 beta-hydroxysteroid dehydrogenase, prior to PMSG injection effectively reduced the PMSG-stimulated increase in the serum estradiol, uterine weight and LH receptors but had no effect on the FSH receptor induction. The ability of PMSG to induce gonadotropin receptors can be arrested at any given time by injecting its antibody, thereby suggesting a continuous need for the hormonal inducer. Estrogen in the absence of the primary inducer was unable to maintain the induced LH and FSH receptor concentration. Inhibition of prostaglandin synthesis using indomethacin aslo had no effect on either the induction or degradation of gonadotropin receptors. Administration of PMSG antiserum, 48 h after PMSG injection, brought about a rapid decline in the induced receptors over the next 24 h, with a rate constant and t 1/2 of 0.078 h-1 and 8.9 h for FSH receptors and 0.086 h-1 and 8.0 h for the LH receptors, respectively.
Mol Cell Endocrinol 1984 Sep
PMID:Effect of pregnant mare serum gonadotropin on the induction and degradation of FSH and LH receptors in the granulosa cell of the immature rat. 609 76

The effect of estrogen on cell proliferation in the descending colon of the mouse as an example of a non-target organ was investigated. Ovariectomized mice were given single or multiple injections of 10 ng/g body weight of 17 beta-estradiol and were killed 1 h after 3H-thymidine injection. Estrogen treatments decreased incorporation of 3H-thymidine into the DNA of colonic mucosa most markedly at 4 h after the single or the last of multiple injections. The inhibitory effect of estrogen on 3H-thymidine incorporation was greater and lasted longer after a single injection than after multiple ones. A similar inhibitory effect was observed in the colonic mucosa of male mice as well as in the mucosa of mice in which colonic epithelial cell proliferation was enhanced by refeeding after 48 h of fasting. However, the colonic mucosa of mice treated with estrogen implants for up to 4 days was not affected. Estrogen treatments caused no significant change in the DNA, RNA and protein contents of the colonic mucosa. The efficacy of estrogen treatments was verified by an increase in both the wet and dry weights of the uterine horns of ovariectomized mice.
Virchows Arch B Cell Pathol Incl Mol Pathol 1981
PMID:Effect of estrogen on cell proliferation in colonic mucosa of the mouse. 616 94

Fluid from large (6-12 mm) porcine follicles (LFFl) enhanced estrogen secretion by granulosa cells from small (1-2 mm) antral porcine follicles during 3-day incubations. Shorter incubations with LFFl or of any length with fluid from small follicles were inconsistent in elevating estrogen secretion. Estrogen was undetectable in freshly collected cells. Addition of 0.14-0.7 micrograms/ml androgens increased estrogen secretion but addition of androgen in a concentration equivalent to that in charcoal-treated LFFl (140 pg/ml) did not. FSH stimulated progesterone but not estrogen secretion. Pretreatment with FSH did not enhance LFFl stimulation of aromatase activity, nor did pretreatment with LFFl influence FSH action on aromatase. These observations suggest the presence of an aromatase stimulator in fluid from nonatretic follicles. By stimulating estrogen production the factor might contribute to follicle development and prevent an increase of the androgen/estrogen ratio which has been proposed to influence atresia.
Mol Cell Endocrinol 1983 Feb
PMID:Follicular fluid stimulation of estrogen secretion by immature porcine granulosa cells. 640 95

Estrogen receptors are present in cytosol prepared from the accessory sex organs (vesicular gland, proprostate, prostate, bulbourethral gland) of sexually immature and of sexually mature rabbits. The receptor in these organs from animals of both age groups has a sedimentation coefficient of 8-10S on low ionic strength (0.01 M KCl) sucrose gradients. Under high ionic strength (0.4 M KCl) conditions, the receptor sediments at approximately 4S. The cytoplasmic estrogen receptor from the epididymis shows age-dependent changes in its sedimentation coefficient. It is 8S under low ionic strength conditions when prepared from immature rabbits and 4S under identical conditions when prepared from sexually mature animals. Although the dissociation constant of the cytoplasmic estrogen receptor in the immature and mature epididymis and accessory sex organs remains constant during development (approximately 0.1 nM), the number of available cytoplasmic estrogen binding sites declines from about 160 fmoles/mg cytosol protein in the immature rabbit to about 40 fmoles/mg cytosol protein in the adult animal. The estrogen receptor in the accessory sex organs is highly specific, the relative affinities of various potential competitors being: estradiol and estrone = 1, diethylstilbestrol = 0.3, estriol = 0.2, tamoxifen = 0.08, testosterone = 0.0004 and 5 alpha-DHT = 0.00005. Changes with age in the physicochemical characteristics of the estrogen receptor and in the concentration of binding sites suggest that the estrogen receptor may be involved in the development and physiological regulation of the male reproductive tract.
Mol Cell Endocrinol 1983 Dec
PMID:Identification of cytoplasmic estrogen receptors in the accessory sex organs of the rabbit and their comparison to the cytoplasmic estrogen receptor in the epididymis. 665 71

We studied DNA synthesis in the rat adenohypophysis during the estrous cycle, pregnancy and lactation. During the estrous cycle, DNA synthesis was 3 times higher on the morning of estrus than on the other days. This peak was abolished completely by ovariectomy or pentobarbital, which also blocked the preovulatory surges of LH and prolactin. Methallibure , which blocked the LH but not the prolaction surge, had a partial effect on DNA synthesis. An acute and significant decrease in pituitary DNA synthesis occurred between days 0 (estrus) and 1 of pregnancy, followed by a less pronounced diminution until parturition. After delivery, DNA synthesis increased steeply on day 1 of lactation, returning to low values by day 3, under normal suckling conditions. Thelectomy , which blocked suckling-induced prolactin release, or antiestrogen treatment, which did not decrease prolactin secretion, diminished pituitary DNA synthesis on day 1 of lactation. Estrogen administration to intact or ovariectomized rats on days 9-11 of lactation stimulated (100%) DNA synthesis. Ovariectomy had no effect. In conclusion, in the different reproductive states studied, pituitary DNA synthesis is related to prolactin release in the presence of estrogens.
Mol Cell Endocrinol 1984 May
PMID:Regulation of pituitary DNA synthesis during different reproductive states in the female rat: role of estrogens and prolactin. 673 26

The hormonal regulation of uterine and oviductal cytoplasmic estrogen and progesterone receptors was studied in immature beagles that were untreated, treated with estradiol-17 beta, or treated sequentially with estradiol and progesterone. Estradiol treatment increased the concentration of estrogen receptors in both tissues. Progesterone receptors were not detectable in the reproductive tract of untreated animals, but increased dramatically under the influence of estradiol. Estrogen withdrawal following estrogen stimulation concomitant estrogen plus progesterone administration, and estrogen withdrawal plus progesterone administration all caused significant reductions in both estrogen and progesterone receptors in uterine oviductal cytosols when compared to estrogen treatment alone. Estrogen withdrawal resembled estrogen plus progesterone administration in reducing both estrogen and progesterone receptor levels, although estrogen withdrawal plus progesterone administration resulted in a further reduction in both receptor concentrations. The same positive and negative relationships between estrogen and progesterone receptor content were observed in uterine cytosols from cycling and ovariectomized adults. These data suggest that estrogen and progesterone regulate their respective receptors and that tissue sensitivity to both steroids may be controlled by mechanisms involving fluctuations in receptor concentration in the reproductive tract of the beagle.
Mol Cell Endocrinol 1981 Feb
PMID:Hormonal regulation of cytoplasmic estrogen and progesterone receptors in the beagle uterus and oviduct. 721 1

Estrogen and progesterone receptors from chick oviduct were compared with respect to their chromatographic behaviour on DEAE-cellulose and their DNA-binding ability to test the general validity of the subunit model from O'Malley and coworkers. Both hormone-receptor complexes can be separated on DEAE-cellulose into 2 components A and B. The 2 progesterone-receptor components appear to occur in equimolar amounts, whereas in the case of the estrogen receptor the amount of component A is always significantly larger. After trypsin treatment the estrogen component B disappears. The remaining A is a receptor fragment with reduced molecular weight. This and other data indicate that the estrogen component B represents an aggregated form of the estrogen receptor and not a receptor subunit. The trypsinated progesterone-receptor fragments, however, are still separable into 2 components, even though also reduced in molecular weight. Our DNA-binding data of the progesterone-receptor components are almost consistent with earlier data from O'Malley and coworkers, even though we find some DNA-binding ability also for component B. Both estrogen-receptor components exhibit affinity for DNA and significantly more than 50% (up to 80%) of the total estrogen-receptor complex are able to bind to DNA. Furthermore we could show that the estrogen-receptor from chick oviduct can be transformed from a DNA-non-binding to a DNA-binding form, similar to other steroid-hormone receptors. This is not compatible with pre-existing receptor subunits in equimolar amounts, one with and the other without affinity for DNA.
Mol Cell Endocrinol 1980 Jul
PMID:The general validity of the subunit model of the progesterone receptor from chick oviduct appears questionable. Comparison of progesterone and estrogen receptor. 739 2

Estrogen receptors (ER) are detected in 50-85% of all breast tumors, and are clinically important because they tend to identify patients with a higher probability of responding to hormonal or endocrine manipulations. However, approximately 30-40% of all ER+ patients do not respond to hormonal manipulations. The lack of response to hormonal manipulations in ER+ patients could be the result of nonfunctional ER, as determined by its inability to recognize and bind to specific DNA-responsive elements and/or its inability to recruit other transcriptional activation factors. The functional status of ER in 34 human breast tumors was assessed determining the structural integrity of the ER DNA-binding domain using site-directed monoclonal anti-estrogen receptor antibody and sucrose density gradient analysis. Based on the fraction of ER containing an intact DNA-binding domain, the tumors were classified into three groups: group I with > 65% of intact ER, group II with > 30% of intact ER, group III with < 30% of intact ER. Clinical and pathologic data were obtained only for patients who were treated with the anti-estrogen tamoxifen and correlated with ER functional status. In group I, 11 of 13 (84.6%) patients were responsive to hormonal therapy with favorable clinical outcome; two patients had unfavorable clinical outcome. In group II, 13 of 15 patients (86.7%) had favourable clinical outcome, and two patients 13.3% had unfavorable outcome. In group III, three of six patients appeared to be hormone responsive with favorable clinical outcome, and three of the patients in this group had unfavorable response to therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Diagn Mol Pathol 1995 Sep
PMID:Estrogen receptor functional status in human breast cancer. 749 42


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