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

Since estrogens have been found to exert a marked inhibitory effect on dopaminergic action at the anterior pituitary and striatal levels in the rat, the effect of estrogen treatment has been studied on the binding characteristics of the dopamine (DA) antagonist [3H]spiroperidol and of the new DA agonist [3H]N-n-propyl-N-phenylethyl-beta-(3-hydroxyphenyl)ethylamine hydrochloride ([3H]RU24213) in rat striatum, nucleus accumbens + olfactory tubercle, frontal cortex and anterior pituitary gland. Specificity of binding was carefully examined in order to investigate possible changes of the agonist and antagonist states of the DA receptor. Estrogen treatment led to a small increase (approx. 20%) of [3H]spiroperidol and [3H]RU24213 binding in rat striatum, nucleus accumbens + olfactory tubercle and frontal cortex while no significant effect was found in the anterior pituitary gland. That the increased binding is due to a corresponding increased number of binding sites and not to higher affinity is indicated by the absence of effect of estrogen treatment on the IC50 values for displacement of the two labeled ligands by a variety of unlabeled compounds. Specificity of binding of DA agonists and antagonists remained unchanged after estrogen treatment. The present data suggest that the potent desensitizing effect of estrogen on DA action at the striatal and pituitary levels is exerted at a step subsequent to binding of DA to its receptor.
Mol Cell Endocrinol 1979 Nov
PMID:Effects of estrogens on the characteristics of [3H]spiroperidol and [3H]RU24213 binding in rat anterior pituitary gland and brain. 11 93

Granulosa cells from preovulatory follicles (PO) or from the enlarged preantral follicles of hypophysectomized immature diethylstilbestrol-treated (Hx-DES) rats were cultured with various combinations of FSH, androst-4-ene-3,17-dione (Ad), estradiol-17beta and dibutyryl cyclic AMP (dbcAMP). Progestin levels (progesterone and 20alpha-dihydroprogesterone) in the medium after 2 days of culture were assayed by radioimmunoassay. The control levels of the two progestins were lower for Hx-DES than for PO cells. Rat FSH (NIAMD-1-3;0.1 mug/ml) caused a 2-fold rise in progestin accumulation in both PO and Hx-DES cultures, dbcAMP (1 mM) increased progestin accumulation in PO cultures 4-5-fold, and to an even greater extent (10-20 fold) in Hx-DES cultures. Androstenedione (1.0 mug/ml) augmented progestin accumulation (1.5-3-fold), and synergized the steroidogenic action of FSH: in cells from Hx-DES rats, combined treatment with FSH and Ad caused a 5-10-fold increase over the values obtained with FSH alone. Testosterone and 5alpha-dihydrotestosterone, but not estradiol-17beta or estrone, mimicked these effects of Ad, Ad did not synergize the action of dbcAMP on progestin levels in Hx-DES cultures. It is proposed that androgen may play a role in the development of the FSH-responsive mechanism in preantral granulosa cells.
Mol Cell Endocrinol
PMID:A synergistic effect of androgen on the stimulation of progesterone secretion by FSH in cultured rat granulosa cells. 18 82

Cultures of granulosa cells from immature hypophysectomized DES-treated rats were unable to maintain progestin production of more than 48 h in medium without hormone supplementation or in the presence of FSH only. Production of progestin (20alpha-dihydroprogesterone, as measured by radioimmunoassay) remained unimpaired in the presence of androstenedione (Ad) and was markedly increased in the presence of both Ad and FSH. The combined treatment with FSH and Ad during the first 48 h of culture brought about persistent changes in the cultured cells, since progestin accumulation did not decline upon subsequent removal of these hormones during days 3 and 4 of culture. Dibutyryl cyclic AMP (DBC) was able to mimic the changes in steroidogenic capability induced by the combined action of FSH and Ad. The extent of [125I]-FSH binding, FSH-stimulable cAMP accumulation and cyclic 3',5'-nucleotide phosphodiesterase activity were not affected by addition of Ad to the culture medium. Ad synergized with DBC in the stimulation of progestin accumulation in granulosa cell cultures. It is suggested that androgen acts at a step in the regulation of progestin biosynthesis distal to cAMP production.
Mol Cell Endocrinol 1977 Sep
PMID:Studies on the synergistic effect of androgen on the stimulation of progestin secretion by FSH in cultured rat granulosa cells: a search for the mechanism of action. 20 May 8

Twenty one UV-sensitive rad mutants were tested for their sensitivity towards DEB. All mutants were more sensitive to this treatment than the wild type. Seven mutants were classified as supersensitive to DEB (rad 1-1, 2,3, 6, 15 and 18-2), while only rad2 and rad3 can be classified as supersensitive to UV. For all mutants ability for liquid holding recovery (LHR) after UV and DEB was compared. Mutants rad 1-1, 3, 5, 6, 9 and 11 differ in their response to LH after the two treatments. Survival of rad1-1 and rad3 increases signficantly during LH after DEB but not after UV exposure. In contrast rad5, 6, 11, and 22 show marked LHR after UV but no increase of survival after DEB treatment.
Mol Gen Genet 1978 Oct 25
PMID:Comparison of sensitivity and liquid holding recovery in rad mutants of Saccharomyces cerevisiae inactivated by UV and DEB. 36 73

Estrogen induces the synthesis and accumulation of the specific messenger RNA for the egg white protein ovalbumin. The messenger RNA has been purified to apparent homogeneity on a preparative scale and utilized to synthesize a radioactive complementary DNA copy. This complementary DNA probe was first used to reveal that although ovalbumin constitutes 60% of the total protein of chick oviduct the gene which codes for the ovalbumin nRNA is represented only once in each haploid genome: The induction of genetranscription and subsequent accumulation of ovalbumin mRNA during estrogen-mediated tissue differentiation was also investigated. Ovalbumin mRNA sequences were quantifiedusing the complementary DNA probe and by an in vitro heterologous translation system. Similar experiments were performed using chicks which were withdrawn from hormone treatment and then given a single injection of estrogen. The data suggest pure transcriptional control for the mechanism by which estrogen regulates the synthesis of the tissuespecific protein ovalbumin. Finally, several in vitro translation systems are comparedwith respect to their usefullness to assess the effects of hormones on mRNA production. It is concluded that the protein synthesis system derived from wheat germ offers thegreatest advantages for initial studies.
Mol Cell Biochem 1975 Apr 30
PMID:Estrogen induction of ovalbumin mRNA: evidence for transcription control. 109 73

The antiestrogen tamoxifen has been successfully used to control estrogen receptor (ER) and progesterone receptor positive breast cancer. However, the development of antiestrogen resistance is frequently observed in patients following long term treatment. We have studied the development of antiestrogen resistance in vitro and established an antiestrogen resistant variant of MCF-7 cells (clone 5C) after long term culture in estrogen free medium. The growth of clone 5C cells was not altered by either estradiol-17 beta or the antiestrogens 4-hydroxytamoxifen and ICI 164,384. Estrogen-stimulated progesterone receptor and reporter gene expression were markedly reduced in 5C cells compared to wild type MCF-7 cells. Only minor alteration in the levels of ER and no alteration in the affinity of ER for ligand were found in 5C cells. No mutation of ER cDNA in 5C cells was detected by polymerase chain reaction and DNA sequencing. This study demonstrates that change(s) in ER-mediated gene expression rather than the amino acid sequence of the ER itself may be associated with the development of at least one form of antiestrogen resistance.
Mol Cell Endocrinol 1992 Dec
PMID:An estrogen receptor positive MCF-7 clone that is resistant to antiestrogens and estradiol. 130

The effect of estrogen on methylation of DNA from the uteri of young (20 weeks) and old (96 weeks) female Wistar rats has been examined by isoschizomeric restriction enzymes and HPLC analysis. In vitro methylation of DNA is significantly higher in the uteri of young rats as compared to old ones. This is reduced by estrogen to greater extent in young than in old age. Furthermore, the digestion of DNA with EcoRI+Msp I shows a distinct 1.2 kb band only in young control. Such band is absent in old control and estrogen-treated sets of both age groups. The HPLC data further reveal that the level of 5-methyl cytosine is high in young and decreases by nearly 18% in old. Estrogen lowers the level of 5-methyl cytosine by 8% in young but shows no effect in the old. Such age-dependent changes in the methylation of DNA brought by estrogen in the rat uterus attribute to alterations in gene expression during aging.
Cell Mol Biol (Noisy-le-grand)
PMID:Methylation of DNA and its modulation by estrogen in the uterus of aging rats. 133 26

The expression of kidney androgen-regulated protein (KAP) gene in mouse kidney is regulated in a multihormonal fashion. As determined by in situ hybridization analysis, epithelial cells of proximal convoluted tubules of cortical nephrons express KAP mRNA in response to androgenic stimulation while similar cells in the juxtamedullary S3 segment of the tubules express KAP mRNA under estrogenic and pituitary hormonal control. In situ hybridization analysis of kidney sections using hypophysectomized (hypox) mice resulted in a total absence of KAP mRNA suggesting the participation of a pituitary hormone(s) in the constitutive expression of KAP mRNA in S3 cells. Treatment of hypox mice with steroid hormones showed that androgens restored the ability of cortical tubule cells to synthesize KAP mRNA. Estrogen treatment, on the other hand, partially induced KAP gene expression only in S3 cells. These results indicated that the androgenic response of the gene is independent of pituitary function, while expression in S3 cells, although partially induced by the direct action of estrogens, is primarily regulated by a pituitary factor. In order to elucidate which hormone(s) is responsible for KAP gene expression in S3 cells, individual pituitary hormones were administered to hypox normal animals and to strains of mice genetically deficient in certain pituitary hormones. Surgically treated C57BL/6 female and male mice were implanted for 7 days with osmotic pumps containing individual pituitary hormones, after which the kidneys were analyzed by in situ hybridization. Mice injected with growth hormone (GH), corticotropin (ACTH), prolactin (PRL), or vehicle failed to express KAP mRNA. Mice treated with thyrotropin (TSH), follitropin (FSH), and lutropin (LH) exhibited high levels of KAP mRNA in S3 cells of females as well as in the renal cortex of male animals. Expression in the cortex in response to LH and FSH may be due to their gonadotropic effect on testosterone production. Similarly, contamination of TSH samples with small amounts of the gonadotropins may explain the cortical response to TSH. TSH produced the strongest response in S3 cells suggesting that it is responsible for the permissive effect of the pituitary on KAP gene expression. This conclusion was supported by studies performed with the dwarf mouse (dw/dw) which lacks PRL, GH, and TSH due to a mutation in the pit-1 gene. In situ hybridization analysis of dwarf mice kidney sections showed a complete lack of KAP gene expression. The possible participation of GH and PRL was eliminated on the basis of the hormone replacement studies.(ABSTRACT TRUNCATED AT 400 WORDS)
Mol Cell Endocrinol 1992 Nov
PMID:Effects of pituitary hormones on the cell-specific expression of the KAP gene. 133 21

Estrogen stimulates uterine epithelial cells to divide, but not estrogen-concentrating neurons in the adult brain. This effect correlates with recent evidence that estrogen can induce the expression of certain growth-related genes in uterus which are not directly induced by estrogen in the adult brain. The possibility that local diffusible factors play a major role in determining tissue-specific effects of estrogen was examined by transplanting uterine tissues into the brain, muscle and kidney of adult rats and then comparing the effects of estrogen on the incorporation of [3H]thymidine and the expression of Fos-, cdc2- and Rb-like immunoreactivity (IR) on native and transplanted uterine tissues, as well as in estrogen-concentrating regions of the brain adjacent to the uterine grafts. In native uteri, estrogen treatment stimulated Fos-, cdc2-, and Rb-like IR, as well as [3H]thymidine incorporation, within lumenal and glandular epithelial cells. All of these effects were estrogen responsive--no immunoreactive staining within uterine epithelial cells and no signs of epithelial cell proliferation were observed in the native uteri of non-estrogen-treated animals. When uterine tissues were transplanted to brain, Fos-, cdc2-, and Rb-like IR epithelial cells, as well as many [3H]thymidine-incorporating uterine epithelial cells, were observed in all estrogen-treated animals and in some non-estrogen-treated animals as well. Identical results were obtained when uterine tissues were transplanted to skeletal muscle, but not to kidney (in the kidney, transplanted epithelial cells expressed all four parameters but only in estrogen-treated animals, comparable to the native uterus). In contrast, estrogen did not stimulate cell division and did not induce Fos-, cdc2-, or Rb-like IR within estrogen-concentrating neuronal regions of the ventromedial hypothalamus. In addition, the presence of uterine tissue in the brain did not confer the ability of estrogen to stimulate any of these parameters within nearby, estrogen-concentrating regions. These data suggest that there are factors in brain and muscle which can allow uterine epithelial cells to divide in the absence of estrogen. There was no evidence of a diffusible factor in brain which inhibits uterine epithelial cell division, nor of a diffusible factor in uterus which can confer estrogenic stimulation of growth-related genes and cell division to central nervous system neurons. In addition, the data provide the first evidence for estrogen regulation of cdc2 and Rb expression in normal uterus.
Mol Cell Endocrinol 1992 Sep
PMID:Role of local environmental factors in determining tissue-specific effects of estrogen: examination of uterine tissues transplanted to brain. 144 88

Estrogen is required for oocyte maturation and embryonic development in vivo; however, the mechanism involved is not clear. Since the effect of estrogen is mediated through the estrogen receptor (ER), we examined the ontogeny and expression of the ER gene in mouse oocytes and embryos of various gestational stages using the highly sensitive reverse transcriptase-polymerase chain reaction (RT-PCR) technique. Total RNA, extracted from 40 ovulated oocytes, 2-cell embryos, morulae, and blastocysts, was reverse transcribed into cDNA. A pair of primers flanking the 453-bp region encoding the hormone-binding domain of ER was used for 30 cycles of PCR. The identity of the amplified product was confirmed by sizing and Southern blot hybridization. The results indicated that ER gene is expressed in unfertilized oocytes and cumulus-oocyte complexes. The amount of ER mRNA decreases in 2-cell embryos, coincident with degradation of maternal mRNA. No ER transcript can be detected in the morulae or blastocyst stage when the embryonic genome has been activated. Postimplantation embryos do not contain detectable ER mRNA until gestation day 8. The levels of ER mRNA increase from day 10 to day 18 of gestation. These data suggest that estrogen, secreted by granulosa cells, may directly influence oocyte growth and maturation in vivo. Since estrogen is known to stimulate the production of growth factors in mouse uteri, the absence of ER mRNA in periimplantation embryos suggests that the effects of estrogen on early embryogenesis may be indirect, i.e., through estrogen-regulated growth-promoting factors produced by the reproductive tract. In mid- and late-post-implantation embryos which contain ER mRNA, estrogen may affect embryonic development through the receptor-mediated mechanisms.
Mol Reprod Dev 1992 Dec
PMID:Expression of estrogen receptor gene in mouse oocyte and during embryogenesis. 147 72


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