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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

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

The regulation of the human androgen receptor (AR) by steroid hormones in human mammary cancer cells was investigated using immunocytochemical and ligand binding assays for its protein and Northern blot analyses for the corresponding mRNA. MFM-223 cells contain high levels of ARs and are growth-inhibited by dihydrotestosterone (DHT). The AR protein is down-regulated to 57% of the control by 10 nM DHT after 24 h, and the corresponding mRNA is also reduced. The nonsteroidal antiandrogen hydroxyflutamide had no effect on the AR level, whereas after incubation with 1 microM cyproterone acetate a slight down-regulation was observed. The AR level was restored completely after release from a 7 day treatment with DHT. However, only 60% of the control level was restored, if the cells wer grown in the presence of DHT for 6 weeks. In androgen-pretreated cells the proliferation rate remained decreased even after the withdrawal of DHT. Concomitantly the distinct growth inhibition was lost. Transfection experiments demonstrated a reduced activity of the residual androgen receptor in these pretreated cells. In addition to the AR, EFM-19 cells also contain significant amounts of estrogen and progesterone receptors. EFM-19 cells are not growth inhibited by physiological concentrations of DHT. Autoregulation of AR was also found in this cell line. Additionally, reduced levels of AR protein and mRNA were found in EFM-19 cells after treatment with the synthetic progestin R5020. The maximum effect of R5020 was observed at the high concentration of 1 microM. Estrogen treatment with 10 nM 17 beta-estradiol for 3 days reduced the AR level only by 25%.
J Steroid Biochem Mol Biol 1992 Dec
PMID:Regulation of androgen receptor mRNA and protein level by steroid hormones in human mammary cancer cells. 147 51

Estrogen destabilizes transferrin mRNA in male Xenopus liver in the same manner as observed for albumin and gamma-fibrinogen. The present study examined estrogen regulation of transferrin gene expression in female Xenopus liver and oviduct. In female Xenopus liver estrogen causes the same enhanced degradation of transferrin mRNA from the cytoplasm as seen in males. In contrast, transferrin is induced 3- to 4-fold in both oviduct nuclear and cytoplasmic RNA. The similar increase in transferrin RNA in both preparations suggests a transcriptional mechanism is responsible for this stimulation. Therefore, transferrin expression is differentially regulated in these tissues by the same hormone. Previous experiments showed that Xenopus serum albumin mRNA has a very short (17 residue) poly(A) tail that may play a role in its hormone-regulated instability. Transferrin mRNA has a similarly short poly(A) tail in liver of both male and female Xenopus. Estrogen has no effect on transferrin polyadenylation in liver. Similarly short poly(A) is found on transferrin mRNA from estrogen-deprived oviducts in explant culture. However, addition of estradiol to the medium results in the appearance of a 50-200 nucleotide poly(A) concurrent with induction. Therefore, transferrin mRNA is differentially polyadenylated in Xenopus liver and oviduct. In the latter tissue polyadenylation is under hormonal control.
J Steroid Biochem Mol Biol 1992 Aug
PMID:Differential regulation and polyadenylation of transferrin mRNA in Xenopus liver and oviduct. 150 5

Studies on hormonal action frequently focus on a single hormone. In intact animals, however, genes may respond to the balance of multiple hormones. Therefore, we have studied the mutual influence of sex steroids on eight genes previously known to be testosterone-responsive in kidneys of mice. A variety of responses to estrogen were recorded. Effects occurred primarily at the transcriptional level although in several cases there was also evidence of decreased mRNA stability. Estrogen did not affect the nuclear location of the androgen receptor. Apparently each gene interacts with both androgen-receptor complex and estrogen-receptor complex, and the ultimate outcome depends on each gene's detailed regulatory structure.
Mol Cell Endocrinol 1992 Aug
PMID:Modulation of androgen-responsive gene expression by estrogen. 151 88


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