Disease relevance of ESR1

• While ER predominantly existed in the prostate stromal cells and the ER mRNA had no difference between the hyperplasia and the normal group [1].
• Androgen- and estrogen-receptor content in spontaneous and experimentally induced canine prostatic hyperplasia [2].
• Estrogen-induced vasodilation was not influenced either by pretreatment with N omega-nitro-L-arginine methyl ester (L-NAME) (100 mumol/liter intracoronary), indomethacin (5 mg/kg body weight intravenously), propranolol (0.75 mg/kg intravenously) or the classic estrogen receptor antagonist ICI 182,780 (10 mumol/liter) [3].
• These results demonstrate that estrogen is cardioprotective against infarct sizes and fatal reperfusion arrhythmias by different ATP-sensitive K(+) channels for an estrogen receptor-independent mechanism [4].
• Tamoxifen (TAM), a nonsteroidal antiestrogen, is approved for use in the treatment of estrogen receptor-positive breast carcinoma and has demonstrated efficacy in chemoprevention of breast cancer in women at high risk for the disease [5].

High impact information on ESR1

• Pretreatment with indomethacin or the classic estrogen-receptor antagonist ICI 182,780 did not alter testosterone-induced changes [6].
• Amelioration of ischemia- and reperfusion-induced myocardial injury by the selective estrogen receptor modulator, raloxifene, in the canine heart [7].
• Raloxifene, a selective estrogen receptor modulator, demonstrates immediate coronary artery vasorelaxing effects [7].
• Acute estrogen-induced dilation in canine coronary arteries is endothelium independent and is not mediated by the classic intracellular estrogen receptor but through non-genomic mechanisms, presumably at the membrane level, which in epicardial arteries may include effects on adenosine triphosphate-sensitive potassium or calcium channels, or both [3].
• An inverse correlation between EGFR and estrogen receptor (ER) was observed in 54% of the tumors [8].

Chemical compound and disease context of ESR1

• In spite of the hormone-dependent nature of this tumor in female Beagles given experimental contraceptive steroids, spontaneous basaloid adenomas lacked estrogen receptor alpha and progesterone receptors [9].
• The purpose of this study is to examine whether raloxifene, one of the selective estrogen receptor modulators, could improve myocardial ischemia and to assess the mechanisms involved [10].

Biological context of ESR1

• Expression of estrogen receptor alpha and beta genes in the mediobasal hypothalamus, pituitary and ovary during the canine estrous cycle [11].
• Increased LH pulse frequency and estrogen secretion associated with termination of anestrus followed by enhancement of uterine estrogen receptor gene expression in the beagle bitch [12].
• The total number of estrogen receptors and nuclear estrogen receptor and its mRNA levels in the uterus also increased (P < 0.01) from late anestrus to proestrus [12].
• In contrast with earlier findings on estrogen receptor-alpha and progesterone receptors, no significant changes in androgen receptor expression were observed during the estrus cycle [13].

Anatomical context of ESR1

• Based on overall staining intensity there appeared to be a higher concentration of ER in the urethra than in the prostate [14].
• In the normal prostate, specific immunocytochemical ER staining was confined to nuclei of the prostatic stroma and prostatic ductal epithelium [14].
• We have used the monoclonal estrogen receptor (ER) antibody H222Sp gamma to localize ER by immunocytochemistry in frozen sections of the normal canine urinary tract of both sexes and of the normal prostate of the male [14].
• In addition to this action, these anti-oestrogens are known to inhibit some types of plasma membrane ion channels and other proteins through mechanisms that do not appear to involve their interactions with the estrogen receptor but could be the result of their effect on membrane lipid structure or fluidity [15].
• In contrast, the basal glands from uteri of CHE group dogs contained more estrogen receptor than glands from normal dogs at the same stage of estrous cycle [16].

Associations of ESR1 with chemical compounds

• Pretreatment with the estrogen-receptor antagonist faslodex (ICI 182,780) did not alter estrogen-induced infarct-limiting and antiarrhythmic effects [4].
• PROCEDURE: ER were detected in formalin-fixed tissues, using an avidin-biotin alkaline phosphatase IHC assay and were quantified on fresh-frozen tumor samples, using a modified dextran-coated charcoal (DCC) assay [17].
• The clonal line which contained measurable ER, had a shift in colony-size distribution to smaller colonies when exposed to tamoxifen or tamoxifen with estradiol that may have been estrogen-receptor mediated [18].
• These effects were partially attenuated by pretreatment with either L-NAME or wortmannin and were completely abolished by ICI182780 (an estrogen receptor antagonist) or L-NAME plus charybdotoxin (a blocker of Ca-activated K channels) [10].
• The number of uterine estrogen receptor and their mRNA levels for ovariectomized bitches were low, but increased (P < 0.05) after treatment with a low dose of estradiol benzoate [12].

Other interactions of ESR1

• A prospective analysis of immunohistochemically determined estrogen receptor alpha and progesterone receptor expression and host and tumor factors as predictors of disease-free period in mammary tumors of the dog [19].

Analytical, diagnostic and therapeutic context of ESR1

• CONCLUSIONS: Immunohistochemistry is an additional method for detection of ER in canine mammary tumors [17].
• The presence of estrogen receptor binding activity in a fraction of canine urine purified by high performance liquid chromatography (HPLC) that did not correspond to estriol, estradiol, estrone or any of their primary metabolites was observed in the present study [20].

References