Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Expression of estrogen receptor gene in mouse oocyte and during embryogenesis. 147 72

The expression and quantitation of the estrogen receptor (ER) in human thyroid tumors were examined by biochemical, immunohistochemical, and reverse transcriptase-polymerase chain reaction (RT-PCR) techniques. For this study, neoplasms, adenomatous goiters and adjacent normal thyroid tissues were obtained from 35 patients which included 10 cases of papillary carcinomas, 17 cases of adenomas and 8 cases of adenomatous goiters. Regardless of the histopathological subtype, ER was detected in 19% (5/27) of the neoplastic tissues with the mean value of ER content of 5.0 +/- 1.3 fmol/mg protein and the mean Kd value of 0.38 +/- 0.28 nM. ER was also detected, but at a lower concentration (2.8 +/- 1.6 fmol/mg protein), in the surrounding normal tissues. There was no significant difference between the neoplasms and adenomatous goiters with respect to the incidence of ER positivity and ER content. Furthermore, ER-positive specimens, as determined by both biochemical and immunohistochemical techniques, also showed the expression of ER mRNA detected by RT-PCR method. These results demonstrate that both ER mRNA as well as ER protein are expressed in thyroid neoplasms. This suggests the possibility that estrogen may affect the tumorigenesis or the progression of some thyroid neoplasms.
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PMID:Expression of the estrogen receptor in human thyroid neoplasms. 752 Dec 73

Human meningiomas are rich in progestin receptors (PR), which are expressed in this tissue in an oestrogen independent fashion. In the search for an explanation of this observation, the existence of a protein in human meningioma cytosol which is capable of binding to a synthetic oestrogen responsive element (ERE) has been demonstrated. Using reverse transcriptase, PCR mRNA encoding for the wild-type oestrogen receptor (ER) was found. In addition, several splice variants of ER mRNA have been identified in human meningioma tissue, including variants lacking exons 4, 5 and 7. We found the ER delta 4 protein to have no transcriptional activity and the ER delta 7 protein reportedly is dominant negative. These mutants therefore probably are not responsible for the autonomous PR synthesis in human meningioma. The ER delta 5 protein, by contrast, has been reported to have oestrogen independent transcriptional activity and it is tempting to speculate that this protein is similar or identical to the ERE binding protein we have found in human meningioma. The role of wild type ER mRNA is presently unclear. Activation of other signal transduction pathways in meningioma does not lead to an increased PR concentration. The promoter area of the meningioma PR gene should be investigated for the possible sensitivity to other transcription factors.
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PMID:Oestrogen receptor independent expression of progestin receptors in human meningioma--a review. 762 81

ER mRNA was detected as 6.0 kb band by Northern blot analysis in vascular smooth muscle cells (VSMC) derived from rat aorta. The presence of ER mRNA in VSMC was confirmed by reverse transcriptase-polymerase chain reaction using specific primers for rat ER cDNA. In addition, the immunocytochemistry of ER was performed in VSMC using a monoclonal anti-ER antibody which recognizes DNA-binding domain of ER. The immunoreactivity was distributed in the cytoplasm as well as in the nuclei. Thus, the expression of ER in VSMC was demonstrated at both the protein and the mRNA level. Furthermore, the expression of c-fos mRNA in VSMC was found up-regulated by 17 beta-estradiol treatment within 30 min. The observation that VSMC possess ER and respond to estrogen supports the idea that estrogen may directly influence vascular cell system through the ER.
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PMID:Vascular smooth muscle cells as target for estrogen. 769 May 60

Recent studies failed to detect estrogen receptors in primate follicles. This study was initiated to determine whether estrogen receptor (ER) messenger ribonucleic acid (mRNA) is present in human granulosa cells and, further, if functional ER proteins are present. To evaluate the presence of ER, RNA from human granulosa cells obtained at the time of oocyte retrieval for assisted reproduction was extracted, and complementary DNA synthesis was performed by the reverse transcriptase-polymerase chain reaction. Oligonucleotide primers were used to amplify basepairs 570-852 in the B- and C- domains of the ER mRNA. Southern blotting was performed and confirmed that the amplified DNA fragment identified in granulosa cells represented ER. By reverse transcriptase-polymerase chain reaction, mRNA for the ER is clearly identified in primary human granulosa cells obtained at the time of oocyte retrieval. To expand these studies and determine whether functional ER were present in human granulosa cells in culture, a simian virus-40-transformed human granulosa cell line was studied. Cells were transfected with a plasmid containing as estrogen response element up-stream from the bacterial reporter gene chloramphenicol acetyltransferase (CAT). In transfected cells, CAT activity is inducible by estradiol if endogenous functional ER are present. In these studies, the transfection analysis confirmed that functional, transcriptionally competent ER are present in a human granulosa cell line, with a 4- to 5-fold enhancement of CAT activity demonstrated after the addition of estradiol compared to that in nonhormone-treated cells. In conclusion, ER mRNA is present in human granulosa cells. Functional ER are also demonstrated in a transformed human granulosa cell line. We hypothesize that low, but biologically significant, amounts of ER protein are present in human granulosa cells, which are not routinely detectable by standard assays.
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PMID:Estrogen receptors are present in human granulosa cells. 782 17

Significant inhibition of proliferative activity in PC3 human prostate cancer cells by estradiol is reported, accompanied by experimental evidence for a specific estrogen receptor (ER). Radioligand-binding assays revealed the presence of high affinity sites of estrogen binding in the nuclear compartment of PC3 cells. In addition, using a reverse transcriptase-polymerase chain reaction system, we obtained evidence of either normal or a variant ER mRNA; the latter, which lacks the entire exon 4, is coexpressed with normal ER mRNA and has been recently characterized in our laboratories. The likelihood that the inhibitory effect exerted by estradiol could be mediated by an increase of transforming growth factor beta (TGF beta) production was also investigated. Use of monoclonal antibodies against TGF beta 1 produced a 3-fold increase of growth rate in PC3 cells; this clearly speaks for high levels of endogenous TGF beta 1. This effect was almost completely abolished after addition of 100 nM estradiol. However, we failed to demonstrate any increase of TGF beta 1 mRNA after estradiol administration using Northern blot analysis. Further studies are needed to ascertain whether the estradiol-induced growth inhibition of PC3 cells is either mediated by other TGF beta species or exerted via alternative mechanism(s).
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PMID:Estradiol inhibits growth of hormone-nonresponsive PC3 human prostate cancer cells. 811 4

Two transcripts of the human estrogen receptor (ER) gene have been described, ER mRNA 1 and mRNA 2, different in their 5' untranslated region. By performing reverse transcriptase-polymerase chain reaction with oligonucleotides specific for the 5' genomic region of the human ER gene we have identified a new ER RNA transcript. The sequence analysis of cDNA from MCF7 breast cancer cells and endometrial human tissues demonstrates that this transcript originates further upstream of the initiation transcription sites so far proposed. Primer extension analysis on RNA from MCF7 cells reveals in the upstream region a possible transcription start site at -3090. In agreement with this result, Northern blot analysis shows, in addition to the canonical 6.3 kb ER mRNA, an ER RNA transcript of approx. 7.4 kb in size. The presence of the additional ER mRNA suggests the existence of a new upstream 5' promoter directing transcription of the human ER gene.
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PMID:Sequencing of an RNA transcript of the human estrogen receptor gene: evidence for a new transcriptional event. 824 Sep 74

We established 17 transplantable rat thyroid tumor cell lines from the primary thyroid tumor of rats induced by N-bis(2-hydroxypropyl)nitrosamine. Among the 17 tumor cell lines established, only two of them (D1 and G1) were estrogen receptor (ER) positive. These two cell lines were characterized with respect to transplantability, histological features, ER contents and cellular localization, and expression of ER message. The ER contents, determined by dextran-coated charcoal assay, were 13.3 and 20.7 fmol/mg protein for D1 and G1 cell lines, respectively. Scatchard plot analysis indicates that the dissociation constants (Kd) were 0.17 and 0.4 nM, respectively, for D1 and G1 cell lines. Sucrose density centrifugation analysis detected a hormone-receptor complex which sedimented at the 4S region, characteristic for ER. Immunohistological staining revealed that the ER was localized in the nuclei. The presence of ER in D1 and G1 cell lines was further confirmed by reverse transcriptase-polymerase chain reaction to detect the ER mRNA. These results demonstrated that ER is expressed in some thyroid tumors. The ER-positive transplantable tumor cell lines are useful for studying the direct effect of estrogen on thyroid tumors in vitro and in vivo.
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PMID:Establishment of estrogen receptor-positive transplantable rat thyroid tumor cell lines in vivo. 836 36

We employed homologous recombination in mouse embryonic stem cells to disrupt the estrogen receptor (ER) gene. Subsequently generated mice that are homozygous for the gene disruption, termed ERKO, possess no demonstrable wild-type ER by Western blot analysis. However, the presence of residual high affinity binding, as detected by [3H]estradiol binding assays and sucrose gradients in uterine extracts from ERKO females prompted further investigation of transcription and translation products from the disrupted ER gene. Analysis of ERKO uterine messenger RNA (mRNA) by reverse transcriptase-polymerase chain reaction demonstrated that although no full-length wild-type ER mRNA was present, two smaller transcripts, labeled E1 and E2, were identified and partially sequenced. Both ERKO transcripts are splicing variants that result in the disrupting NEO sequence being partially or completely removed from the mRNA. In the ERKO-E2 variant, this results in a frame shift and the creation of at least two stop codons downstream. In the ERKO-E1 variant, the ER reading frame is preserved and encodes for a smaller mutant ER that could be the source of the residual estradiol binding. When this mutant form is overexpressed and characterized in vitro, it results in a smaller protein of the predicted size that possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER. Despite residual amounts of an impaired ER variant, estrogen insensitivity in the female ERKOs was confirmed by the failure of estrogen treatment to induce known uterine markers of estrogen action, such as increased DNA synthesis, and transcription of the progesterone receptor, lactoferrin, and glucose-6-phosphate dehydrogenase genes. Furthermore, serum levels of estradiol in the ERKO female are more than 10-fold higher than those in the wild type, consistent with a syndrome of hormone insensitivity.
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PMID:Analysis of transcription and estrogen insensitivity in the female mouse after targeted disruption of the estrogen receptor gene. 858 21

In normal estrogen target tissues, estrogen action is mediated through a specific nuclear transcription factor, the estrogen receptor (ER). The site of estrogen action in the developing organism is therefore determined by cells that contain ER and other necessary tissue and gene-specific components for estrogen-mediated transcription. Immunocytochemical methods were used to determine the cellular localization and tissue distribution of ERs in reproductive tracts of mouse fetuses. Nuclear staining for ER was observed in reproductive tracts at fetal days 13 to 15. ERs were present in the precursors of both male and female reproductive tracts at these early developmental stages, which may be attributable to their similar embryonic origins. However, as the tissues undergo sexual differentiation at later fetal and early neonatal ages, ER increases in the female reproductive tracts as compared with the male. ER was detected by immunoblotting on fetal day 10 (before sexual differentiation) in extracts of whole mouse embryos. To determine whether ER and progesterone receptor genes are expressed earlier in development, we examined RNA from preimplantation mouse embryos using reverse transcriptase-polymerase chain reaction techniques. ER mRNA was found in oocytes and fertilized eggs. Message concentration declined at the 2-cell stage and reached its lowest level at the 5- to 8-cell stage. ER mRNA was not detectable at the morula stage but reappeared at the blastocyst stage. Progesterone receptor mRNA was not detectable until the blastocyst stage. The embryonic expression of ER and progesterone receptor genes in the blastocyst suggests a possible functional requirement for estrogen and progesterone receptors in preimplantation embryos.
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PMID:Embryonic estrogen receptors: do they have a physiological function? 859 78


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