scholarly journals Classical GenotropicVersusKinase-Initiated Regulation of Gene Transcription by the Estrogen Receptor α

Endocrinology ◽  
2006 ◽  
Vol 147 (4) ◽  
pp. 1986-1996 ◽  
Author(s):  
M. Almeida ◽  
L. Han ◽  
C. A. O’Brien ◽  
S. Kousteni ◽  
S. C. Manolagas
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Estrogen Receptor Α

Sp1 is essential for estrogen receptor α gene transcription

2002 ◽  
Vol 82 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Linda A. deGraffenried ◽  
Susan G. Hilsenbeck ◽  
Suzanne A.W. Fuqua
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Α Gene

scholarly journals Estrogen Receptor (ER)-β Reduces ERα-Regulated Gene Transcription, Supporting a “Ying Yang” Relationship between ERα and ERβ in Mice

2003 ◽  
Vol 17 (2) ◽  
pp. 203-208 ◽  
Author(s):  
Marie K. Lindberg ◽  
Sofia Movérare ◽  
Stanko Skrtic ◽  
Hui Gao ◽  
Karin Dahlman-Wright ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Physiological Role ◽  
Estrogen Receptor Α ◽  
Mrna Levels ◽  
Wild Type ◽  
Ovariectomized Mice ◽  
Adult Bone

Abstract Estrogen is of importance for the regulation of adult bone metabolism. The aim of the present study was to determine the role of estrogen receptor-β (ERβ) in vivo on global estrogen-regulated transcriptional activity in bone. The effect of estrogen in bone of ovariectomized mice was determined using microarray analysis including 9400 genes. Most of the genes (95% = 240 genes) that were increased by estrogen in wild-type (WT) mice were also increased by estrogen in ERβ-inactivated mice. Interestingly, the average stimulatory effect of estrogen on the mRNA levels of these genes was 85% higher in ERβ-inactivated than in WT mice, demonstrating that ERβ reduces estrogen receptor-α (ERα)-regulated gene transcription in bone. The average stimulatory effect of estrogen on estrogen-regulated bone genes in ERα-inactivated mice was intermediate between that seen in WT and ERαβ double-inactivated mice. Thus, ERβ inhibits ERα-mediated gene transcription in the presence of ERα, whereas, in the absence of ERα, it can partially replace ERα. In conclusion, our in vivo data indicate that an important physiological role of ERβ is to modulate ERα-mediated gene transcription supporting a “Ying Yang” relationship between ERα and ERβ in mice.

Estrogen receptor-α: molecular mechanisms and interactions with the ubiquitin proteasome system

2010 ◽  
Vol 1 (1) ◽  
pp. 1-9
Author(s):  
Vladimir Stanišić ◽  
David M. Lonard ◽  
Bert W. O'Malley
Keyword(s):  
Estrogen Receptor ◽  
Molecular Biology ◽  
Gene Transcription ◽  
Molecular Mechanisms ◽  
Hormone Treatment ◽  
Ubiquitin Proteasome System ◽  
Estrogen Receptor Α ◽  
Receptor Protein ◽  
Ubiquitin Proteasome ◽  
The 1960S

AbstractEstrogen receptor-α (ERα) is a protein with a long history of study that precedes the advent of modern molecular biology. Over the course of 50 years, ERα has been increasingly recognized as a prominent model for the study of the mechanism of gene transcription in vertebrates. It also serves as a regulatory molecule for numerous physiological and disease states. Several fundamental insights have been made using ERα as a model protein, from the discovery that endocrine hormones elicit gene transcription to our understanding of the relationship between ERα-mediated transcription and transcription factor degradation by the ubiquitin proteasome system (UPS). Understanding of receptor protein degradation developed alongside other aspects of its molecular biology, from early observations in the 1960s that ERα is degraded on hormone treatment to the current understanding of ERα transcriptional regulation by the UPS. Here, we present the concept of ERα turnover from the perspective of the historical development of this notion and highlight some of the latest discoveries regarding this process. We discuss the logic and significance of ERα degradation pathways in the context of cell and whole-organism homeostasis.

scholarly journals Poly(ADP-ribose) Polymerase 1 Is a Key Regulator of Estrogen Receptor α-dependent Gene Transcription

2013 ◽  
Vol 288 (16) ◽  
pp. 11348-11357 ◽  
Author(s):  
Fengxiao Zhang ◽  
Yan Wang ◽  
Lin Wang ◽  
Xi Luo ◽  
Kun Huang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Gene Transcription ◽  
Estrogen Receptor Α

scholarly journals Anacardic Acid Inhibits Estrogen Receptor α–DNA Binding and Reduces Target Gene Transcription and Breast Cancer Cell Proliferation

2010 ◽  
Vol 9 (3) ◽  
pp. 594-605 ◽  
Author(s):  
David J. Schultz ◽  
Nalinie S. Wickramasinghe ◽  
Margarita M. Ivanova ◽  
Susan M. Isaacs ◽  
Susan M. Dougherty ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Dna Binding ◽  
Gene Transcription ◽  
Target Gene ◽  
Estrogen Receptor Α ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Target Gene Transcription

scholarly journals The AF-1 Activation Function of Estrogen Receptor α Is Necessary and Sufficient for Uterine Epithelial Cell Proliferation In Vivo

Endocrinology ◽  
2013 ◽  
Vol 154 (6) ◽  
pp. 2222-2233 ◽  
Author(s):  
Anne Abot ◽  
Coralie Fontaine ◽  
Isabelle Raymond-Letron ◽  
Gilles Flouriot ◽  
Marine Adlanmerini ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Epithelial Cell ◽  
Gene Transcription ◽  
Crucial Role ◽  
Estrogen Receptor Α ◽  
Epithelial Cell Proliferation ◽  
Wild Type

Abstract Estrogen receptor-α (ERα) regulates gene transcription through the 2 activation functions (AFs) AF-1 and AF-2. The crucial role of ERαAF-2 was previously demonstrated for endometrial proliferative action of 17β-estradiol (E2). Here, we investigated the role of ERαAF-1 in the regulation of gene transcription and cell proliferation in the uterus. We show that acute treatment with E2 or tamoxifen, which selectively activates ERαAF-1, similarly regulate the expression of a uterine set of estrogen-dependent genes as well as epithelial cell proliferation in the uterus of wild-type mice. These effects were abrogated in mice lacking ERαAF-1 (ERαAF-10). Four weeks of E2 treatment led to uterine hypertrophy and sustained luminal epithelial and stromal cell proliferation in wild-type mice, but not in ERαAF-10 mice. However, ERαAF-10 mice still presented a moderate uterine hypertrophy essentially due to a stromal edema, potentially due to the persistence of Vegf-a induction. Epithelial apoptosis is largely decreased in these ERαAF-10 uteri, and response to progesterone is also altered. Finally, E2-induced proliferation of an ERα-positive epithelial cancer cell line was also inhibited by overexpression of an inducible ERα isoform lacking AF-1. Altogether, these data highlight the crucial role of ERαAF-1 in the E2-induced proliferative response in vitro and in vivo. Because ERαAF-1 was previously reported to be dispensable for several E2 extrareproductive protective effects, an optimal ERα modulation could be obtained using molecules activating ERα with a minimal ERαAF-1 action.

1322: The Expression of Estrogen Receptor α and Estrogen Receptor β in the Human Fetal Prostate

2004 ◽  
Vol 171 (4S) ◽  
pp. 348-348
Author(s):  
Ellen Shapiro ◽  
Hongying Huang ◽  
Rachael R. Mash ◽  
Eliza Ng ◽  
Deborah E. McFadden ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Β
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