Estrogen-induced downregulation of TASK-1 expression through estrogen receptor β in N2A cells
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Estrogen receptor beta
Estrogen receptor alpha
Estrogen receptor beta
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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)
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Progesterone receptor
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GPER
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Abstract Human breast cancer can be divided into a group that contains specific receptor sites for estrogen and a group without such specific estrogen‐binding sites. The presence of specific estrogen receptors in some tumors indicating hormonal dependency has been shown to be of predictive value for endocrine treatment. This would greatly improve therapeutic planning for patients with breast cancer. Tumor tissue from 52 patients was investigated for content of both cytosol estrogen and estrogen receptor. In addition, the total tumor estrogen was also determined in 14 of these tumors. The results of this investigation show two distinct groups: one group containing both estrogen receptor and estrogen and a second group with no receptor but with measurable amount of estrogen. Tumors with estrogen receptors have higher tissue levels of estrogen than tumors without specific estrogen receptor. Even in the absence of estrogen receptor, however, most tumor tissue examined contained a measurable amount of estrogen.
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The definition of the role of estrogen is a long-date scientific preoccupation. On the basis of the studies carried out in the last twenty years, it is now well accepted that estradiol and its cognate receptors are relevant transcription regulators in reproductive as well as non-reproductive tissues. Models of estrogen (E2) insufficiency (ArKO) and estrogen receptors (ER) dysfunction (ERKOs) have revealed new and unexpected roles of estradiol and its receptors both in female and male. The purpose of this study is to use mouse models of estrogen insufficiency (ArKO) and estrogen receptors dysfunction (ERKOs) to provide a genomic insight in the multiple and complex mechanisms defining estrogenic signaling to help understanding its role in physiological and pathological conditions. In particular the objective was to identify the genes responsive to estrogen signaling according to various possible mechanisms: 1) estrogen and estrogen receptordependent actions; 2) estrogen-independent and estrogen-receptor-dependent actions; 3) estrogen receptor-independent estrogen-dependent actions. To reach this aim, estrogen and estrogen receptors dependent genes expression profiling were performed by microarray analysis in ventral and dorso-lateral prostate and gonadal white adipose tissue from mouse models of impaired estrogen synthesis (ArKO) and ER action (ERKOs). The experimental and biological reproducibility of microarray data was first verified and confirmed providing a correlation between real-time PCR and microarrays in fold change measurements and in expression profiles across all tissues. The results obtained from the analysis of the expression profiles indicate that the classical and the non-genomic actions of estrogen are not to represent the main mechanisms of estrogenic signaling in prostate and adipose tissue. Conversely it appears that the estrogenic signaling in these tissues is exerted via estrogen receptors with an estrogen-independent mechanism of action. ERa appear to be the main mediator of the observed estrogenic effects, with mechanisms that differ according to the specific tissue. In ventral and dorso-lateral prostates, ERa seems to have inhibitory effects on transcription of target genes, supporting the hypothesis of its implication as a tumor suppressor in the prostate gland. Additional studies need to be performed to permit the identification of genes whose regulation can be directly modulated by ERs.
Estrogen receptor alpha
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PELP-1
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Estrogen receptors are important for the development and maintenance of many different tissues in the body including the breast, uterus, brain and bone. There are two known genes encoding estrogen receptors, Estrogen Receptor alpha (ERα) and Estrogen Receptor beta (ERβ). These receptors are transcription factors with distinct functional domains involved in DNA binding, ligand binding and transcriptional regulation. A novel isoform of human ERβ (ERβ548) which includes an extended amino terminal domain has been identified. Isoform specific antibodies confirm the presence of this receptor in human tissue. Transactivation analysis with different estrogenic ligands indicates that ERβ548 is functionally distinct from previously reported forms of ERβ.
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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.
Estrogen receptor alpha
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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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