scholarly journals The expression of aromatase, estrogen receptor a and estrogen receptor b in mouse Leydig cells in vitro that derived from cryptorchid males

10.4081/928 ◽  
2009 ◽  
Vol 49 (1) ◽  
pp. 59 ◽  
Author(s):  
M Kotula-Balak ◽  
M Gancarczyk ◽  
J Sadowska ◽  
B Bilinska
Keyword(s):  
Estrogen Receptor ◽  
Leydig Cells

Estrogen Receptor-Mediated Transcription In Vitro

1999 ◽  
Author(s):  
Hong Liu ◽  
Virgil C. Jordan
Keyword(s):  
Estrogen Receptor ◽  
Transcription In Vitro

In vivo and in vitro phosphorylation of the human estrogen receptor

1995 ◽  
Vol 52 (2) ◽  
pp. 159-171 ◽  
Author(s):  
Steven F. Arnold ◽  
John D. Obourn ◽  
Matthew R. Yudt ◽  
Timothy H. Carter ◽  
Angelo C. Notides
Keyword(s):  
Estrogen Receptor ◽  
Human Estrogen Receptor

scholarly journals Agonists and knockdown of estrogen receptor β differentially affect invasion of triple-negative breast cancer cells in vitro

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Susanne Schüler-Toprak ◽  
Julia Häring ◽  
Elisabeth C. Inwald ◽  
Christoph Moehle ◽  
Olaf Ortmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Estrogen Receptor Β

scholarly journals Effect of antagonists on DNA binding properties of the human estrogen receptor in vitro and in vivo.

1995 ◽  
Vol 9 (5) ◽  
pp. 579-591 ◽  
Author(s):  
D Metzger ◽  
M Berry ◽  
S Ali ◽  
P Chambon
Keyword(s):  
Estrogen Receptor ◽  
Dna Binding ◽  
Binding Properties ◽  
Human Estrogen Receptor ◽  
Dna Binding Properties

Dibutyltin (DBT) inhibits in vitro androgen biosynthesis of rat immature Leydig cells

Toxicology ◽  
2021 ◽  
pp. 152779
Author(s):  
Guoping Li ◽  
Xiuting Chang ◽  
Daoyuan Li ◽  
Xinli Kang
Keyword(s):  
Leydig Cells

scholarly journals The treatment effects of flaxseed-derived secoisolariciresinol diglycoside and its metabolite enterolactone on benign prostatic hyperplasia involve the G protein-coupled estrogen receptor 1

2016 ◽  
Vol 41 (12) ◽  
pp. 1303-1310 ◽  
Author(s):  
Guan-Yu Ren ◽  
Chun-Yang Chen ◽  
Wei-Guo Chen ◽  
Ya Huang ◽  
Li-Qiang Qin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Estrogen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
G Protein ◽  
Therapeutic Potential ◽  
Prostatic Hyperplasia ◽  
Docking Simulations ◽  
G Protein Coupled

Secoisolariciresinol diglucoside (SDG), a lignan extracted from flaxseed, has been shown to suppress benign prostatic hyperplasia (BPH). However, little is known about the mechanistic basis for its anti-BPH activity. The present study showed that enterolactone (ENL), the mammalian metabolite of SDG, shared the similar binding site of G1 on a new type of membranous estrogen receptor, G-protein-coupled estrogen eceptor 1 (GPER), by docking simulations method. ENL and G1 (the specific agonist of GPER) inhibited the proliferation of human prostate stromal cell line WPMY-1 as shown by MTT assay and arrested cell cycle at the G0/G1 phase, which was displayed by propidium iodide staining following flow cytometer examination. Silencing GPER by short interfering RNA attenuated the inhibitory effect of ENL on WPMY-1 cells. The therapeutic potential of SDG in the treatment of BPH was confirmed in a testosterone propionate-induced BPH rat model. SDG significantly reduced the enlargement of the rat prostate and the number of papillary projections of prostatic alveolus and thickness of the pseudostratified epithelial and stromal cells when comparing with the model group. Mechanistic studies showed that SDG and ENL increased the expression of GPER both in vitro and in vivo. Furthermore, ENL-induced cell cycle arrest may be mediated by the activation of GPER/ERK pathway and subsequent upregulation of p53 and p21 and downregulation of cyclin D1. This work, in tandem with previous studies, will enhance our knowledge regarding the mechanism(s) of dietary phytochemicals on BPH prevention and ultimately expand the scope of adopting alternative approaches in BPH treatment.

scholarly journals Ligand-dependent repression of the erythroid transcription factor GATA-1 by the estrogen receptor.

1995 ◽  
Vol 15 (6) ◽  
pp. 3147-3153 ◽  
Author(s):  
G A Blobel ◽  
C A Sieff ◽  
S H Orkin
Keyword(s):  
Bone Marrow ◽  
Estrogen Receptor ◽  
Transcription Factor ◽  
Progenitor Cells ◽  
Erythroid Cell ◽  
High Dose ◽  
Dependent Manner ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells

High-dose estrogen administration induces anemia in mammals. In chickens, estrogens stimulate outgrowth of bone marrow-derived erythroid progenitor cells and delay their maturation. This delay is associated with down-regulation of many erythroid cell-specific genes, including alpha- and beta-globin, band 3, band 4.1, and the erythroid cell-specific histone H5. We show here that estrogens also reduce the number of erythroid progenitor cells in primary human bone marrow cultures. To address potential mechanisms by which estrogens suppress erythropoiesis, we have examined their effects on GATA-1, an erythroid transcription factor that participates in the regulation of the majority of erythroid cell-specific genes and is necessary for full maturation of erythrocytes. We demonstrate that the transcriptional activity of GATA-1 is strongly repressed by the estrogen receptor (ER) in a ligand-dependent manner and that this repression is reversible in the presence of 4-hydroxytamoxifen. ER-mediated repression of GATA-1 activity occurs on an artificial promoter containing a single GATA-binding site, as well as in the context of an intact promoter which is normally regulated by GATA-1. GATA-1 and ER bind to each other in vitro in the absence of DNA. In coimmunoprecipitation experiments using transfected COS cells, GATA-1 and ER associate in a ligand-dependent manner. Mapping experiments indicate that GATA-1 and the ER form at least two contacts, which involve the finger region and the N-terminal activation domain of GATA-1. We speculate that estrogens exert effects on erythropoiesis by modulating GATA-1 activity through protein-protein interaction with the ER. Interference with GATA-binding proteins may be one mechanism by which steroid hormones modulate cellular differentiation.

Neuroprotective effects of an estratriene analog are estrogen receptor independent in vitro and in vivo

2005 ◽  
Vol 1038 (2) ◽  
pp. 216-222 ◽  
Author(s):  
Evelyn Perez ◽  
Ran Liu ◽  
Shao-Hua Yang ◽  
Zu Yun Cai ◽  
Douglas F. Covey ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Neuroprotective Effects
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