Disease relevance of LOC407238

• Estrogen receptor-alpha mediates estradiol attenuation of ATP-induced Ca2+ signaling in mouse dorsal root ganglion neurons [1].
• Both the gene transfer of estrogen receptor alpha using adenovirus and treatment with the protein kinase C inhibitor bisindolylmaleimide I significantly enhanced the effects of 17beta-E2 treatment under high-glucose conditions, whereas these effects were abolished by the estrogen receptor antagonist ICI 182,780 (faslodex) [2].
• Evaluation of potential implication of membrane estrogen binding sites on ERE-dependent transcriptional activity and intracellular estrogen receptor-alpha regulation in MCF-7 breast cancer cells [3].

High impact information on LOC407238

• We found that suppression of GPR30 but not ER-alpha prevented E2-BSA- or E2-induced PKA activation and Bcl-2 expression [4].
• At 2 hours after trauma-hemorrhage, administration of E2-conjugated to bovine serum albumin (E2-BSA, membrane impermeable) or E2 induced the up-regulation of ER-alpha and GPR30 and attenuated hepatic injury [4].
• We propose a new model of ligand-independent activation of estrogen receptors in which the level of phosphorylation of ERalpha, and hence its transcriptional activation, is determined by the net effect of these counterregulatory pathways [5].
• We now report that ERalpha-dependent gene expression also is regulated by protein phosphatase 2A (PP2A) [5].
• It has recently been shown that kinase-mediated phosphorylation of ERalpha also transcriptionally activates the receptor in the absence of estrogen [5].

Chemical compound and disease context of LOC407238

• Transient inhibition of synergistically insulin-like growth factor-1- and bisphenol A-induced poliferation of estrogen receptor alpha (ERalpha)-positive human breast cancer MCF-7 cells by melatonin [6].

Biological context of LOC407238

• ERalpha bound to a palindromic estrogen response element (ERE) and two half-site EREs; mutation of any of these sites decreased basal expression and completely obliterated E2 stimulation [7].
• Stimulation of the novel estrogen receptor-alpha intronic TERP-1 promoter by estrogens, androgen, pituitary adenylate cyclase-activating peptide, and forskolin, and autoregulation by TERP-1 protein [7].
• We examined the hypothesis that human estrogen receptor-alpha (ER alpha) gene transfection improves the endothelial cell function [8].
• Using pmAb 1D5, the mean percentage of ERalpha-positive caruncular stromal cells decreased from 39.0% +/- 5.9% in pregnant cows to 17.5% +/- 8.3% at parturition (P = 0.011) [9].
• Occurrence of estrogen receptor alpha in bovine placentomes throughout mid and late gestation and at parturition [9].

Anatomical context of LOC407238

• From these results, we concluded that estrogens down-regulate l-glu uptake activity of astrocytes via membrane ERalpha [10].
• Only pmAb recognizing the C-terminus identified ERalpha in the caruncular epithelium, in which positive reactions were found in all cells, with the exception of areas adjacent to the chorionic plate and to major chorionic villi, where the specific signal gradually faded and occasionally disappeared [9].
• Both types of pmAbs identified ERalpha in stromal cells and capillary pericytes of the maternal caruncular septae [9].
• This study demonstrates that the nongenomic and short-term effect of E(2) on endothelial NO release is Ca(2+)-dependent and occurs via ERalpha localized in plasmalemmal caveolae [11].
• Expression and localization of estrogen receptor alpha, estrogen receptor beta and progesterone receptor in the bovine oviduct in vivo and in vitro [12].

Associations of LOC407238 with chemical compounds

• Estrogens inhibit l-glutamate uptake activity of astrocytes via membrane estrogen receptor alpha [10].
• 16alpha-Iodo-17beta-estradiol (16alphaIE2), an estrogen receptor alpha (ERalpha) selective ligand, revealed an inhibitory effect at 10 nm, while genistein, an ERbeta selective ligand, failed to reveal such an effect at this concentration [10].
• Pituitary estrogen receptor alpha and dopamine subtype 2 receptor gene expression in transgenic mice with overproduction of heterologous growth hormones [13].
• The partial antagonist tamoxifen did not block E(2)-induced NO production; however, a pure estrogen receptor alpha (ERalpha) antagonist ICI 182,780 completely inhibited E(2)-stimulated NO release [11].
• Expression of estrogen receptor alpha and 17beta-hydroxysteroid dehydrogenase 4 in the ciliary body [14].

Other interactions of LOC407238

• Further discrimination between the estrogen receptor subtypes alpha and beta revealed the expression of the estrogen receptor beta, whereas for the estrogen receptor alpha no reproducible positive signal could be obtained with the available antibodies [15].
• Specific ovine ERalpha and bovine ERbeta cDNA probes were labeled with [-32S]dCTP [16].
• Endometrial concentrations of ERalpha and PGHS-2 mRNA transcripts were greater on d 7 than on d 3 of the estrous cycle, but did not differ between treatments [17].
• Distribution of estrogen receptor alpha in the dominant follicles and corpus luteum at the three stages of estrous cycle in Japanese black cows [18].

Analytical, diagnostic and therapeutic context of LOC407238

• The expression of ERalpha in bovine placentomes was further confirmed by the detection of ERalpha-specific mRNA by reverse transcriptase-polymerase chain reaction and by Western blot analysis [9].
• Mammary epithelial proliferation and estrogen receptor alpha expression in prepubertal heifers: effects of ovariectomy and growth hormone [19].
• To detect ERalpha and 17beta-HSD4 transcripts, reverse transcription-polymerase chain reaction (RT-PCR) was used [14].
• ERalpha was visualized by immunohistochemistry on paraffin sections of ovaries obtained from 11 non-pregnant and 2 pregnant animals [20].

References