Estrogen associated gene polymorphisms and their interactions in the progress of Alzheimer's disease
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Estrogen receptor alpha
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Estrogen receptor beta
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The purpose of this article is to present an assessment of the expression levels of estrogen receptors ER-alpha and ER-beta in malicious tumors of the uterine corpus.Estrogen receptor expression levels were tested using semiquantitative immunohistochemical methods. Paraffin-embedded sections of tissue from the corpus of the uterus from 171 patients were used in the research.Analysis of the relation between ER-beta expression levels and the clinical grade of disease (based on FIGO classification) showed that these parameters are significantly related: p = 0.0099. There were no statistically significant relations between ER-alpha expression levels in tumors or clinical stages of tumors based on the FIGO criteria. The presence of high estrogen receptor beta expression levels is often accompanied by a low estrogen receptor alpha expression level and such arrangements allow the overt biological function of a dominant receptor.The differences in tissue distribution of both estrogen receptors could indicate their different biological roles.
Estrogen receptor alpha
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Alpha (finance)
BETA (programming language)
Progesterone receptor
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Estrogen receptor beta
Estrogen receptor alpha
GPER
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Estrogen receptors (ER) are members of the nuclear receptor superfamily of ligand-activated transcription factors and mediate the effects of estrogen on target tissues. ERalpha was the first estrogen receptor to be characterized, and ERbeta was identified ten years later. The role of ERbeta in breast cancer pathobiology is largely unknown because specific antibodies have not been available until recently. The purpose of this study was to explore the expression of ERbeta in breast neoplasms and to correlate it with ERalpha and prognosis. ERa and ERbeta expression was monitored immunohistochemically in 59 breast carcinomas. We found no correlation between ERalpha and ERbeta expression, between ERbeta expression and the known prognostic indicators such as tumor size, grade or lymph node status, or between ERbeta expression and survival. Our findings contribute to the better understanding of the role of ERbeta in breast cancer.
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The role of the estrogen receptor in the regulation of reproductive functions as well as its localization in reproductive tissues is well established. The estrogen receptor subtypes namely estrogen receptor alpha (ESR1) and estrogen receptor beta (ESR2) are the mediators of the physiological responses that are brought about by estrogens. Various mouse models such as the ESR1, ESR2 and ESR1/2 knock-outs have been developed to determine the function of these receptors. Although the reproductive abnormalities of these mouse models have been well characterized, there is limited literature about transgenic mice that were specifically generated to serve as models of endocrine disruption in the ovary. Recently, we generated a transgenic mouse model in which ESR1 is overexpressed in several tissues (ESR1 OE), including the ovaries. The goal is to use these mice as models for endocrine disruption in the ovary. Previous studies using quantitative real-time PCR determined that the mRNA levels of ESR1 were significantly higher in the ESR1 OE mice compared to controls. The unique feature of this model is that it was designed using the doxycycline responsive system, thus giving us the ability to regulate the overexpression of ESR1 by administering doxycycline via food to the mice. In our previous experiment, doxycycline (200 mg/kg) was administered to the mice via food for 5 days. The results showed that there were no differences in the mRNA levels between ESR1 OE and controls, hence confirming that doxycycline treatment did indeed shut-off overexpression of ESR1. Although our ultimate goal is to determine whether overexpression of ESR1 during development results in aberrant responses to endogenous hormones or exogenous chemicals later as adults, it is necessary to first characterize this mouse model to build a foundation to design future experiments. Since ESR1 can regulate transcription of several genes, we hypothesized that ESR1 OE in the ovary alters expression of ESR2, aryl hydrocarbon receptor (AhR), androgen receptor (AR), progesterone receptor (PR), luteinizing hormone receptor (LHR) as well as follicle-stimulating hormone receptor (FSHR). The ovaries of the ESR1 OE and controls were isolated and subjected to quantitative real-time PCR using primers for the receptors. The results indicate that the mRNA levels of ESR2 were significantly lower in the ESR1 OE ovaries compared to the controls (control = 1.14 ± 0.02 genomic equivalents (ge); ESR1 OE = 0.47 ± 0.01 ge; n = 3; p ≤ 0.05). The mRNA levels of AhR as well as AR were significantly higher in ESR1 OE compared to controls (AhR mRNA levels in control = 0.23 ± 0.02 ge; ESR1 OE = 0.49 ± 0.09 ge; n = 4; p ≤ 0.05; AR mRNA levels in control = 0.78 ± 0.08 ge; ESR1 OE = 1.13 ± 0.23 ge; n = 4; p ≤ 0.05). However, the mRNA levels of PR, LHR and FSHR in ESR1 OE were not significantly different from controls (PR mRNA levels in control = 0.92 ± 0.54 ge; ESR1 OE = 0.92 ± 0.82 ge; n = 4; p = 0.1; LHR mRNA levels in control = 0.42 ± 0.36 ge; ESR1 OE = 0.42 ± 0.15 ge; n = 4; p = 0.65; FSHR mRNA levels in control = 1.18 ± 0.18 ge; ESR1 OE = 1.37 ± 0.26 ge; n = 4; p = 0.27). These data suggest possible cross-talk between ESR1 and AhR as well as AR in gene regulation. Support: NIH R21ES13061
Estrogen receptor alpha
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Raloxifene
Estrogen receptor beta
Hormone response element
Estrogen receptor alpha
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Abstract Estrogen is of importance for the regulation of adult bone metabolism. The aim of the present study was to determine the role of estrogen receptor-β (ERβ) in vivo on global estrogen-regulated transcriptional activity in bone. The effect of estrogen in bone of ovariectomized mice was determined using microarray analysis including 9400 genes. Most of the genes (95% = 240 genes) that were increased by estrogen in wild-type (WT) mice were also increased by estrogen in ERβ-inactivated mice. Interestingly, the average stimulatory effect of estrogen on the mRNA levels of these genes was 85% higher in ERβ-inactivated than in WT mice, demonstrating that ERβ reduces estrogen receptor-α (ERα)-regulated gene transcription in bone. The average stimulatory effect of estrogen on estrogen-regulated bone genes in ERα-inactivated mice was intermediate between that seen in WT and ERαβ double-inactivated mice. Thus, ERβ inhibits ERα-mediated gene transcription in the presence of ERα, whereas, in the absence of ERα, it can partially replace ERα. In conclusion, our in vivo data indicate that an important physiological role of ERβ is to modulate ERα-mediated gene transcription supporting a “Ying Yang” relationship between ERα and ERβ in mice.
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Hormone response element
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Estrogen receptors(ERs),belonging to the nuclear receptor superfamily,mainly include ER-α66,ER-α36,ER-α46 and ER-β.Each of them performs specific functions by binding to its ligand such as estrogen.Recently,ER-α36,a novel variant of human estrogen receptor-alpha(ER-α) was identified and cloned.ER-α36 primarily localizes to the plasma membrane and cytoplasma and inhibits the transactivation of both ER-α66 and ER-β.Being predominantly a membrane-based ER,it mediates non-genomic estrogen signaling and involves in resistance to endocrine therapy such as tamoxifen in breast cancer.
Estrogen receptor alpha
Estrogen receptor beta
Estrogen-related receptor gamma
PELP-1
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Estrogen receptor alpha
Estrogen receptor beta
Estrogen-related receptor gamma
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