International Union of Pharmacology. LXIV. Estrogen Receptors

Dahlman-Wright, Karin; Cavaillès, Vincent; Fuqua, Suzanne A.W.; Jordan, V. Craig; Katzenellenbogen, John A.; Korach, Kenneth S.; Maggi, Adriana; Muramatsu, Masami; Parker, Malcolm G.; Gustafsson, Jan Åke

doi:10.1124/pr.58.4.8

Cited by 500 publications

(400 citation statements)

References 92 publications

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“…One explanation could be that BPA may act via ER through mechanisms other than binding to ERE. For instance, it may act through other transcription factors binding to their respective response elements (Dahlman-Wright et al, 2006). In addition, it has been demonstrated that extra-nuclear ER can activate protein kinases (Giretti et al, 2008;Migliaccio et al, 1996;Simoncini et al, 2000).…”

Section: E2 and Bpa Are Equally Effective Through A Non-classical Estmentioning

confidence: 99%

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

Nadal

Alonso-Magdalena

Soriano

et al. 2009

Molecular and Cellular Endocrinology

265

187

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. The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes. Molecular and Cellular Endocrinology, Elsevier, 2009, 304 (1-2) Please cite this article as: Nadal, A., Alonso-Magdalena, P., Soriano, S., Quesada, I., Ropero, A.B., The pancreatic ␤-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. THE PANCREATIC -CELL AS A TARGET OF ESTROGENS AND XENOESTROGENS: IMPLICATIONS FOR BLOOD GLUCOSE HOMEOSTASIS AND DIABETESAngel Rosen & Spiegelman, 2006;Fritsche et al., 2008). During the fasting state, insulin remains at low levels because plasma glucose concentration is low. In this situation, the levels of the counter-regulatory hormones, glucagon, adrenaline and corticosteroids are increased to promote hepatic glucose production. In contrast, insulin, the only hormone in the body able to decrease blood glucose levels, is increased during the fed state. Insulin decreases blood glucose by promoting adipocyte and muscle glucose uptake, as well as by preventing the liver from producing glucose by suppressing glycogenolysis and gluconeogenesis (Fritsche et al., 2008). neurotransmitters, hormones and nutrients, among which glucose is the most important.Normally, in response to short glucose stimulation, insulin biosynthesis is regulated by the increased translation of the preproinsulin transcript. After a prolonged glucose exposure, however, it is regulated via the insulin gene transcription (Orland et al., 1985;Permutt & Rotwein, 1983;Poitout et al., 2006). Both transcriptional and translational regulation of insulin biosynthesis is essential to maintain the intracellular stores of insulin on a long term basis.The secretory response of -cells depends on their electrical activity. This consists of oscillations of the membrane potential that range from electrically silent periods to depolarised plateaus on which Ca 2+ -action potentials originate (Rorsman et al., 2000).The classical stimulus-secretion coupling that drives insulin release involves the closure of K ATP channels by increasing the intracellular ATP/ADP ratio (Ashcroft et al., 1984) and diadenosine polyphosphates concentration (DPs) (Ripoll et al., 1996) oscillatory pattern is originated (Nadal et al., 1999;Santos et al., 1991;Valdeolmillos et al., 1989), which triggers a pulsatile insulin secretion (Barbosa et al., 1998;Gilon et al., 1993;Dyachok et al., 2008). Estrogens, estrogen receptors and blood glucose homeostasisT...

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Section: E2 and Bpa Are Equally Effective Through A Non-classical Estmentioning

confidence: 99%

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

Nadal

Alonso-Magdalena

Soriano

et al. 2009

Molecular and Cellular Endocrinology

265

187

View full text Add to dashboard Cite

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“…In the nucleus, ERs undergo conformational changes upon interaction with estrogen (E2), allowing them to bind DNA and promote transcription of target genes. 7,8 In addition to direct transcriptional effects, ERs localized to the plasma membrane can influence the activity of signalling pathways through coupling directly or indirectly to G-proteins by non-genomic mechanisms. 7 This leads to activation of downstream effectors such as protein kinase C-d, 9 mitogen activated protein kinase ERK (MAPK) 9,10,11 and phosphatidylinositol-3-OH kinase (PI3K).…”

Section: Introductionmentioning

confidence: 99%

RASSF1A inhibits estrogen receptor alpha expression and estrogen-independent signalling: implications for breast cancer development

et al. 2012

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The Ras association domain family 1 isoform A (RASSF1A) is a tumor suppressor whose inactivation is implicated in the development of many human cancers, including breast carcinomas. Little is known about the tumor-suppressive function of RASSF1A in breast tissue and whether its inactivation is mechanistically involved in the initiation and progression of breast tumors. Here, we show that RASSF1A inhibits breast cancer growth in vivo, and suppresses estrogen receptor (ERa) expression and function. Reconstitution of RASSF1A in MCF7 cells led to decreased ERa levels and reduced sensitivity to estrogen (E2). Concomitantly, we observed decreased expression of Id1 as well as the E2-responsive genes Bcl-2 and c-Myc that cooperatively contribute to the immortalization and transformation of breast epithelial cells. This downregulation was associated with induction of cell-cycle arrest and senescence that constitute early barriers to cancer initiation and progression. Knockdown of ERa showed that downregulation of ERa suffices to increase senescence and inhibit expression of Bcl-2, c-Myc and Id1. However, enforced expression of ERa only partially rescued RASSF1A-mediated growth inhibition and senescence, suggesting that suppression of ERa expression and activity is not the only mechanism by which RASSF1A inhibits growth and survival of breast cancer cells. Ectopic expression of Bcl-2, c-Myc and Id1 had little or no effect on RASSF1A-mediated growth arrest, indicating that RASSF1A acts dominantly over these oncogenes. Mechanistically, RASSF1A was found to suppress ERa expression through Akt1. It also transiently inhibited ERa-induced Ras-MAPK activity after exposure of cells to E2. Together, our data show that RASSF1A acts as a tumor suppressor in ERa þ mammary epithelial cells, in part through inhibiting ERa expression and activity. These findings suggest that RASSF1A has a key role in suppressing the transformation of human breast epithelial cells and ERa þ breast cancer initiation.

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“…While ERs are master regulators essential for development and maintenance of normal sexual and reproductive functions, they can also play a role in the cardiovascular, musculoskeletal, immune and central nervous systems. [8][9][10] These two diverse networks exhibit crosstalk that can be due to direct interaction between p53 and the ERs, with the more frequently described outcome being repression of p53 activity, [11][12][13][14] although p53 can also inhibit ERα. 15,16 The inhibitory crosstalk, which can be mediated by physical interactions between the two proteins, can be relieved by stress-dependent post-translational modifications of p53.…”

Section: Interaction Between P53 and Estradiol Pathways In Transcriptmentioning

confidence: 99%

Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics

Lion¹,

Bisio²,

Tebaldi³

et al. 2013

Cell Cycle

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International Union of Pharmacology. LXIV. Estrogen Receptors

Cited by 500 publications

References 92 publications

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

RASSF1A inhibits estrogen receptor alpha expression and estrogen-independent signalling: implications for breast cancer development

Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics

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