Disease relevance of ESR1

• Chimeric VTGII-CAT genes were cotransfected into LMH chicken hepatoma cells along with an estrogen receptor expression vector, and transient CAT expression was assayed after culturing the cells in the absence or presence of estrogen [1].
• Superinfection resistance studies suggest that the variant virus recognizes the subgroup B receptor on chicken cells and the subgroup E receptor on quail cells [2].
• Using a combination of in vivo and in vitro studies we have analyzed the interactions of the estrogen receptor with genes from three different systems: the long terminal repeat (LTR) of the mouse mammary tumor virus (MMTV), the chicken and xenopus vitellogenin genes and the rabbit uteroglobin gene [3].

High impact information on ESR1

• This paper describes an estrogen receptor which is found in both the nucleus and cytoplasm of liver cells from male Xenopus laevis, and which seems to be involved in the induction of vitellogenin synthesis [4].
• The kinetics of estrogen-receptor binding to chromatin indicate that these sites are saturated within 15 min of estrogen administration to the chicks, demonstrating that the lag is not due to slow uptake of the steroid [5].
• It binds to the nuclear estrogen receptor and is antagonized by the antiestrogen tamoxifen [6].
• To induce self-renewal, the GR required the continuous presence of an activated receptor tyrosine kinase and had to cooperate with the estrogen receptor for full activity [7].
• The molecules identified comprised receptor tyrosine kinases (c-Kit and c-ErbB) and members of the nuclear hormone receptor superfamily (thyroid hormone receptor and estrogen receptor) [7].

Biological context of ESR1

• About 2%-6% of thyroid-stimulating-hormone-immunopositive and 1%-2% prolactin-immunopositive cells expressed ERalpha at later stages of embryonic development, but no growth-hormone-positive or adrenocorticotropic-hormone-positive cells expressed ERalpha during the embryonic period [8].
• The proportion of ERalpha(+) cells in the pituitary was about 6% at E8.5; expression increased to 22% by E18.5 of gestation, with no additional change until hatching [8].
• The first highly conserved ER region is not present in the truncated v-erbA gene, but shares some homology with the N-terminal end of the GR [9].
• A chicken oviduct cDNA clone containing the complete open reading frame of the oestrogen receptor (ER) has been isolated and sequenced [9].
• The three guanine residues in each half of the palindrome are protected against methylation by dimethylsulfate after incubation with ER, but not with glucocorticoid (GR) or progesterone (PR) receptors [10].

Anatomical context of ESR1

• Thus, gonadotrophs are the main cell population expressing ERalpha in the anterior pituitary gland of chick embryo, and ERalpha is involved in regulating the development of the pituitary gland and the maturation of the hormone-secreting function [8].
• Ontogeny of estrogen receptor (ER) alpha and its co-localization with pituitary hormones in the pituitary gland of chick embryos [8].
• Estrogen receptor immunoreactivity was found only in the nuclei of glandular epithelial cells [11].
• Here we show that upon incubation with the purified estrogen receptor (ER) from calf uterus the Xenopus vitellogenin A2 gene yields a DNase-I footprint over the ERE between -331 and -319 [10].
• A coincident increase in nuclear estrogen receptor and decrease in cytosol estrogen receptor 2 to 4 h postoviposition was suggestive of in vivo receptor translocation [12].

Associations of ESR1 with chemical compounds

• Double-labeling of ERalpha and pituitary hormones showed that the dominant cell types expressing ERalpha were gonadotrophs immunopositive for luteinizing hormone (LH); the proportion of ERalpha(+) cells expressing LH increased throughout gestation and reached approximately 57% at hatching [8].
• Progesterone and estradiol participate in the regulation of several reproductive functions through interaction with intracellular progesterone receptors (PR) and estrogen receptors (ER), respectively [13].
• An increase in the chicken ER mRNA levels was observed 24 h after stimulation with progesterone [14].
• In vivo secondary stimulation of chicken oviduct total RNA with diethylstilbestrol does not induce chicken ER mRNA [14].
• Furthermore we could show that the estrogen-receptor from chick oviduct can be transformed from a DNA-non-binding to a DNA-binding form, similar to other steroid-hormone receptors [15].

Physical interactions of ESR1

• Depleting the estradiol receptors from the cell and nuclear extracts by means of estradiol-receptor antibodies covalently bound to Matrex beads reduced the stimulation of the vitellogenin gene by 40% [16].
• Previous studies showed that VBP can bind simultaneously with the estrogen receptor to the putative complex regulatory element E1D [17].

Regulatory relationships of ESR1

• Although most of these mutations compromised VTGII promoter function, one dramatically increased expression in LMH cells and also rendered the VTGII promoter capable of being activated by cis-linked EREs in fibroblasts cotransfected with an estrogen receptor expression vector [1].
• Estrogen receptor gene transfection induced ovalbumin mRNA to a moderate extent in the absence of the steroid hormones [18].

Other interactions of ESR1

• Changes in the content of progesterone receptor isoforms and estrogen receptor alpha in the chick brain during embryonic development [13].
• A known estrogen-inducible protein, ovalbumin, was localized in the same glandular epithelial cells as ER [11].
• The estrogen action on the expression of avidin could be explained by estrogen-induced terminal differentiation of the epithelial gland cells or by a direct effect of estrogen on the progesterone action, for instance interaction of estrogen receptor and progesterone receptor in the regulation of transcription [19].
• DNA-cellulose competition binding assays were used to measure the ability of cloned DNA fragments of the chicken vitellogenin II gene to displace the estrogen-receptor complex from total chicken DNA coupled to cellulose [20].
• Estrogen receptor in hen oviduct chromatin, digested by micrococcal nuclease [21].

Analytical, diagnostic and therapeutic context of ESR1

• We therefore followed, by immunohistochemistry, the ontogeny of the pituitary ER alpha (ERalpha), and the cell types expressing ERalpha throughout chick embryo development [8].
• In this work, we determined PR and ER-alpha isoforms content in the brain of chicks of both sexes on days 8 and 13 of embryonic development as well as on the day of hatching by Western blot analysis [13].
• The aim of this study was to detect the presence of estrogen receptor alpha in different cell subpopulations of the growing left and regressing right ovaries from newly hatched chicks, by immunohistochemical methods, using an indirect immunoperoxidase technique [22].
• After binding of the salt-activated estradiol-receptor complex to DNA-cellulose in the cold, an increase of its sedimentation constant and its size, as measured by density-gradient centrifugation and agarose gel chromatography, resp., becomes apparent [23].
• Degenerate PCR primers specific to ER were designed and used to amplify alligator ovary RNA [24].

References