Human oestrogen receptor cDNA: sequence, expression and homology to v-erb-A

Green, Stephen; Walter, P.; Kumar, Vijay; Krust, Andrée; Bornert, Jean‐Marc; Argos, Patrick; Chambon, Pierre

doi:10.1038/320134a0

Cited by 2,175 publications

(982 citation statements)

References 44 publications

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“…The adaptor introduced a BamHI site and destroyed one of the XhoI sites. In order to construct a vector encoding an estrogen-inducible Myb protein [RED(ERMYB)] the estrogen binding domain of the human estrogen receptor (amino acids 282 ± 576) (Green et al, 1986) was ligated into the BamXI ± XhoI cleaved vectors. A non-hormone inducible control for use in chloramphenicol acetyltransferase (CAT) assays was constructed by inserting the viral oncogene v-myb into the pUC13 plasmid downstream of the long terminal repeat of Schmidt-Ruppin strain of Rous Sarcoma Virus (nucleotide residue 8 ± 376) (Gorman, 1985).…”

Section: Plasmid Constructionmentioning

confidence: 99%

Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2

et al. 1997

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Primary murine fetal hemopoietic cells were transformed with a fusion protein consisting of the ligand-binding domain of the estrogen receptor and a carboxylterminally truncated c-Myb protein (ERMYB). The ERMYB-transformed hemopoietic cells exhibit an immature myeloid phenotype when grown in the presence of b-estradiol. Upon removal of b-estradiol, the ERMYB cells display increased adherence, decreased clonogenicity and di erentiate to cells exhibiting granulocyte or macrophage morphology. The expression of the c-myc, ckit, cdc2 and bcl-2 genes, which are putatively regulated by Myb, was investigated in ERMYB cells grown in the presence or absence of b-estradiol. Neither c-myc nor cdc2 expression was down-regulated after removal of bestradiol demonstrating that di erentiation is not a consequence of decreased transactivation of these genes by ERMYB. While bcl-2 expression was reduced by 50% in ERMYB cells grown in the absence of bestradiol, there was no increase in DNA laddering, suggesting that Myb was not protecting ERMYB cells from apoptosis. In contrast, a substantial (200-fold) decrease in c-kit mRNA level was observed following di erentiation of ERMYB cells, and c-kit mRNA could be partially re-induced by the re-addition of b-estradiol. Furthermore, a reporter construct containing the c-kit promoter was activated when cotransfected with a Myb expression vector, providing further evidence of a role for Myb in the regulation of c-kit.

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Section: Plasmid Constructionmentioning

confidence: 99%

Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2

et al. 1997

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“…Estrogens exert the majority of their actions on target cells interacting with two specific estrogen receptors (ESR1 and ESR2), 7,8 while progestogens interact with the progesterone receptor (PGR), 9 therefore genetic variations in these genes may also be important to prediction of risks associated with HRT.…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor 2 and progesterone receptor gene polymorphisms and lipid levels in women with different hormonal status

et al. 2004

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Sex steroid hormones have multiple effects on lipid metabolism. We investigated the association between two common single nucleotide polymorphisms of the estrogen receptor 2 gene (ESR2), 1082G4A and 1730A4G, and PROGINS polymorphism of the progesterone receptor gene (PGR) with lipoprotein levels in a cross-sectional study with 472 women of European descent. The women were classified into three subgroups according to hormonal status, premenopausal women (n ¼ 187; mean age ¼ 3479.7 years), postmenopausal women exposed to hormone replacement therapy (HRT) (n ¼ 118; 5676.7 years) and postmenopausal women unexposed to HRT (n ¼ 167; 5879.8 years). The premenopausal and postmenopausal women exposed to HRT, both carriers of G/A genotype, exhibited LDL-C (P ¼ 0.027 and 0.001, respectively) and T-chol levels (P ¼ 0.035 and 0.001, respectively) lower than carriers of G/G genotype. This association was not observed in postmenopausal women unexposed to HRT. These results suggest that ESR2 1082G4A genotype may influence LDL-C levels in women with abundant estrogen levels, due to either endogenous or exogenous sources. INTRODUCTIONEndogenous and exogenous sex steroid hormones have multiple effects on lipid and lipoprotein metabolism. The oral estrogen replacement therapy (ERT) in postmenopausal women decreases serum total cholesterol (T-chol) and lowdensity lipoprotein cholesterol (LDL-C) concentrations, as well as increases serum high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels. 1 The effects of combined (estrogen plus progestin) hormone replacement therapy (HRT) are uncertain; the addition of a progestogen to estrogens tends to attenuate the increase in serum HDL-C and the decrease in LDL-C, obtained with ERT, although this effect seems to be related to the dose and to androgenic potency of the progestogen. 2 The beneficial changes in these lipoproteins should be associated with at least 30-35% decline in coronary heart disease (CHD) incidence. 3 However, the results from the Heart and Estrogen/Progestin Replacement Study (HERS) 4 and the Women's Health Initiative (WHI) trial 5 demonstrated that oral HRT does not provide cardiovascular benefit or even some evidence of cardiovascular harm.

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“…E2 is known to control the development of the reproductive tract and mammary gland, regulate the oestrus cycle, control lactation, and exert regulatory influences important for bone, liver, and cardiovascular systems, as well as behaviour. The critical regulatory functions of oestrogen are mediated by oestrogen receptors (ERs) and at least two types of oestrogen receptors, ERα and ERβ, are known in mammals (Green et al 1986;Kuiper et al 1996). The molecular mechanisms of ER transactivation have been well characterized.…”

Section: Introductionmentioning

confidence: 99%

Genome‐wide analysis of changes in early gene expression induced by oestrogen

et al. 2002

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Background: The sex hormone 17β‐oestradiol (E2) has profound effects on many aspects of reproduction, development, as well as behaviour. Although the oestrogen receptor is well characterized on a molecular level, relatively few genes affected by E2 have been identified, and the mechanisms underlying the physiological changes caused by E2 are largely unknown. In order to identify oestrogen‐regulated genes in vivo, early uterine gene expression profiles were developed using DNA microarrays. Results: Ovariectomized mice were exposed to 17β‐oestradiol for 6 h, and mRNA expression analysis for 9977 genes was performed. Although a large number of genes was affected by oestrogen administration, the genes that showed higher reproducibility in repetitive experiments were selected and further examined. For most of the selected genes, expression was induced in a dose‐dependent manner, and gene expression was not altered following oestrogen treatment in oestrogen receptor‐α (ERα)‐deficient mice. In combination with the estimation of gene expression levels using quantitative PCR, it was revealed that multiple genes related to sterol biosynthesis, tRNA synthesis, RNA processing, and growth signalling were activated. Based on the microarray data, we selected additional genes related to sterol biosynthesis and tRNA synthesis and confirmed that these genes are also activated by oestrogen. Conclusion: Genes suggesting a basis for the drastic uterotrophic effect observed several days following oestrogen administration were identified. These findings not only reveal the diverse effect of oestrogen signalling on transcript levels in vivo but also demonstrate the ability of DNA microarrays to identify cellular pathways affected by oestrogen.

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Human oestrogen receptor cDNA: sequence, expression and homology to v-erb-A

Cited by 2,175 publications

References 44 publications

Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2

Inactivation of a c-Myb/estrogen receptor fusion protein in transformed primary cells leads to granulocyte/macrophage differentiation and down regulation of c-kit but not c-myc or cdc2

Estrogen receptor 2 and progesterone receptor gene polymorphisms and lipid levels in women with different hormonal status

Genome‐wide analysis of changes in early gene expression induced by oestrogen

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