A second estrogen receptor from Japanese lamprey (Lethenteron japonicum) does not have activities for estrogen binding and transcription

The lability of estrogen receptor: correlation of estrogen binding and immunoreactivity.

Clinical Chemistry ◽

10.1093/clinchem/32.9.1774 ◽

1986 ◽

Vol 32 (9) ◽

pp. 1774-1777 ◽

Cited By ~ 5

Author(s):

F Clayton ◽

J Wu

Keyword(s):

Estrogen Receptor ◽

Enzyme Immunoassay ◽

Dextran Coated Charcoal ◽

Reagent Cost ◽

Estrogen Binding

Abstract We compared the Abbott enzyme immunoassay method for estrogen receptor with a standard dextran-coated charcoal method, and studied the effects of treatments causing denaturation. Estrogen receptor values were slightly higher by the Abbott method, but the methods agreed with regard to receptors being present or absent in 94-98% of 50 cases. Heat lability of immunoreactivity by the Abbott enzyme immunoassay is comparable to the lability of estrogen binding by the estrogen receptor. Estrogen and molybdate substantially stabilized estrogen receptor during the assay, but improper handling of tissue before the assay may cause similar, substantial decreases in estrogen receptor by either method. The Abbott method is easier to use than the dextrancoated charcoal method, requires less tissue, and measures receptor with or without endogenously bound estrogen, but reagent cost is high.

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Estrogen Receptor-Independent Catechol Estrogen Binding Activity: Protein Binding Studies in Wild-Type, Estrogen Receptor-α KO, and Aromatase KO Mice Tissues†

Biochemistry ◽

10.1021/bi036154j ◽

2004 ◽

Vol 43 (21) ◽

pp. 6698-6708 ◽

Cited By ~ 17

Author(s):

Brian J. Philips ◽

Pete J. Ansell ◽

Leslie G. Newton ◽

Nobuhiro Harada ◽

Shin-Ichiro Honda ◽

...

Keyword(s):

Estrogen Receptor ◽

Protein Binding ◽

Estrogen Receptor Α ◽

Binding Activity ◽

Wild Type ◽

Binding Studies ◽

Catechol Estrogen ◽

Estrogen Binding

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Estrophilin immunoreactivity versus estrogen receptor binding activity in meningiomas: Evidence for multiple estrogen binding sites

Surgical Neurology ◽

10.1016/0090-3019(87)90131-5 ◽

1987 ◽

Vol 28 (3) ◽

pp. 181-188 ◽

Cited By ~ 6

Author(s):

K.P. Lesch ◽

W. Schott ◽

S. Gross

Keyword(s):

Estrogen Receptor ◽

Receptor Binding ◽

Binding Sites ◽

Binding Activity ◽

Estrogen Receptor Binding ◽

Receptor Binding Activity ◽

Estrogen Binding

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Antioxidants and Gene Regulation: The Effects of Vitamins C and E on Estrogen Receptors

Elements ◽

10.6017/eurj.v2i1.8970 ◽

2006 ◽

Vol 2 (1) ◽

Author(s):

Jeong Ho Nam

Keyword(s):

Breast Cancer ◽

Nitric Oxide ◽

Estrogen Receptor ◽

Breast Cancer Cells ◽

Past Research ◽

Receptor Expression ◽

Cancer Development ◽

Nitric Oxide Release ◽

Gene Level ◽

Estrogen Binding

Research shows that estrogen binding to its receptor plays a role in breast cancer development and that antioxidants possibly mitigate this effect. Past research examined whether various treatments lead to accelerated cell division, but characterization and comparison of the effects of different treatments on gene level expression of the receptor was not accomplished. Initially, the effect of antioxidants on the estrogen receptor expression was investigated, revealing the presence of Vitamins C and E on nitric oxide release (a possible cancer reduction agent) stimulated by estrogen acting on the surface estrogen receptor of breast cancer cells was observed. Generally, Vitamin E was most effective for improving nitric oxide release.

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Involvement of estrogen receptors α and β in the regulation of cervical permeability

AJP Cell Physiology ◽

10.1152/ajpcell.2000.278.4.c689 ◽

2000 ◽

Vol 278 (4) ◽

pp. C689-C696 ◽

Cited By ~ 20

Author(s):

George I. Gorodeski ◽

Dipika Pal

Keyword(s):

Estrogen Receptor ◽

Binding Sites ◽

Estrogen Receptor Α ◽

Binding Activity ◽

Scatchard Analysis ◽

Single Class ◽

Estrogen Receptor Modulators ◽

Transcription Inhibitor ◽

Estrogen Binding ◽

In Cells

Estrogen increases the permeability of cultured human cervical epithelia (Gorodeski, GI. Am J Physiol Cell Physiol 275: C888–C899, 1998), and the effect is blocked by the estrogen receptor modulators ICI-182780 and tamoxifen. The objective of the study was to determine involvement of estrogen receptor(s) in mediating the effects on permeability. In cultured human cervical epithelial cells estradiol binds to high-affinity, low-capacity sites, in a specific and saturable manner. Scatchard analysis revealed a single class of binding sites with a dissociation constant of 1.3 nM and binding activity of ∼0.5 pmol/mg DNA. Estradiol increased the density of estrogen-binding sites in a time- and dose-related manner (half time ≈ 4 h, and EC50≈ 1 nM). RT-PCR assays revealed the expression of mRNA for the estrogen receptor α (αER) and estrogen receptor β (βER). Removal of estrogen from the culture medium decreased and treatment with estrogen increased the expression of αER and βER mRNA. In cells not treated with estrogen, ICI-182780 and tamoxifen increased βER mRNA. In cells treated with estrogen, neither ICI-182780 nor tamoxifen had modulated significantly the increase in αER or βER mRNA. The transcription inhibitor actinomycin D blocked the estrogen-induced increase in permeability, and it abrogated the estradiol-induced increase in estrogen binding sites. These results suggest that the estrogen-dependent increase in cervical permeability is mediated by an αER-dependent increase in transcription.

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