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Article ; Online: AhR and ARNT modulate ER signaling.

Swedenborg, Elin / Pongratz, Ingemar

2010 Volume 268, Issue 3, Page(s) 132–138

Abstract: The aryl hydrocarbon receptor (AhR), in complex with its binding partner ARNT, mediates the cellular response to xenobiotic compounds such as the environmental pollutant dioxin. In addition, the AhR has important regulatory roles in normal physiology. ... ...

Abstract	The aryl hydrocarbon receptor (AhR), in complex with its binding partner ARNT, mediates the cellular response to xenobiotic compounds such as the environmental pollutant dioxin. In addition, the AhR has important regulatory roles in normal physiology. For instance, there is extensive data showing an intricate relationship between the AhR and estrogen receptor (ER) pathways. This review focuses on the regulatory roles of AhR and ARNT, beyond the response to xenobiotics. In particular, the effects of AhR agonists on the estrogen signaling pathways and the role of ARNT as a modulator of ER activity are discussed.
MeSH term(s)	Animals ; Aryl Hydrocarbon Receptor Nuclear Translocator/agonists ; Aryl Hydrocarbon Receptor Nuclear Translocator/antagonists & inhibitors ; Aryl Hydrocarbon Receptor Nuclear Translocator/physiology ; Endocrine Disruptors/toxicity ; Environmental Pollutants/toxicity ; Humans ; Methylcholanthrene/toxicity ; Polychlorinated Dibenzodioxins/toxicity ; Receptors, Aryl Hydrocarbon/agonists ; Receptors, Aryl Hydrocarbon/antagonists & inhibitors ; Receptors, Aryl Hydrocarbon/physiology ; Receptors, Estrogen/drug effects ; Receptors, Estrogen/physiology ; Signal Transduction/physiology ; Xenobiotics/metabolism ; Xenobiotics/toxicity
Chemical Substances	ARNT protein, human ; Endocrine Disruptors ; Environmental Pollutants ; Polychlorinated Dibenzodioxins ; Receptors, Aryl Hydrocarbon ; Receptors, Estrogen ; Xenobiotics ; Aryl Hydrocarbon Receptor Nuclear Translocator (138391-32-9) ; Methylcholanthrene (56-49-5)
Language	English
Publishing date	2010-02-09
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2009.09.007
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Zs.A 888: Show issues

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Article ; Online: Endocrine disruptive chemicals: mechanisms of action and involvement in metabolic disorders.

Swedenborg, Elin / Rüegg, Joëlle / Mäkelä, Sari / Pongratz, Ingemar

Journal of molecular endocrinology

2009 Volume 43, Issue 1, Page(s) 1–10

Abstract: Endocrine disruption refers to the ability of chemicals to interfere with hormonal systems, and has raised considerable concern in recent years. Endocrine disruptive chemicals (EDCs) pose a documented risk to wildlife and have the potential to negatively ...

Abstract	Endocrine disruption refers to the ability of chemicals to interfere with hormonal systems, and has raised considerable concern in recent years. Endocrine disruptive chemicals (EDCs) pose a documented risk to wildlife and have the potential to negatively influence human health. This review focuses on the molecular mechanisms of endocrine disruption and the possible involvement of EDCs in metabolic disorders. The first part describes the role of aryl hydrocarbon receptor (AhR) and nuclear receptors (NRs) in mediating effects of EDCs, in particular, how cross-talk between AhR and NR pathways can lead to endocrine disruption. The second part deals with how these receptors are involved in metabolic functions and how their targeting by EDCs can lead to disturbances in glucose and fat metabolism. The article illustrates that, although there is accumulating data on molecular mechanisms of EDC action as well as on EDC involvement in metabolic disorders, there is still a great demand for data that can unite the mechanistic and the toxicological/epidemiological observations.
MeSH term(s)	Animals ; Endocrine Disruptors/poisoning ; Endocrine Disruptors/toxicity ; Humans ; Metabolic Diseases/chemically induced ; Receptors, Cell Surface/metabolism
Chemical Substances	Endocrine Disruptors ; Receptors, Cell Surface
Language	English
Publishing date	2009-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1677/JME-08-0132
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Article: The aryl hydrocarbon receptor ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene regulate distinct genetic networks

Swedenborg, Elin / Kotka, Maria / Seifert, Martin / Kanno, Jun / Pongratz, Ingemar / Rüegg, Joëlle

Molecular and cellular endocrinology. 2012 Oct. 15, v. 362, no. 1-2

2012

Abstract: The two estrogen receptor isoforms ERα and ERβ mediate biological effects of estrogens, but are also targets for endocrine disruptive chemicals (EDCs), compounds that interfere with hormonal signaling. 3-Methylcholanthrene (3-MC) and dioxin (TCDD) are ... ...

Abstract	The two estrogen receptor isoforms ERα and ERβ mediate biological effects of estrogens, but are also targets for endocrine disruptive chemicals (EDCs), compounds that interfere with hormonal signaling. 3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling. However, in contrast to TCDD, 3-MC gives rise to metabolites with estrogenic properties. We compared gene expression profiles in HepG2 cells after exposure to 3-MC, TCDD, and the synthetic estrogen diethylstilbestrol (DES). Interestingly, we observed little overlap between the genetic networks activated by 3-MC and TCDD, two compounds sometimes considered as interchangeable AhR ligands. Like DES, 3-MC induced a number of ER-regulated genes and lead to recruitment of ERα to the promoters of such genes. Interestingly, in contrast to DES, the estrogenic effects exerted by 3-MC were exclusively observed in ERα, but not in ERβ-expressing cells, suggesting ER isoform selectivity of 3-MC-derived metabolites.
Keywords	agonists ; diethylstilbestrol ; estrogen receptors ; estrogenic properties ; gene expression ; genes ; human cell lines ; metabolites ; tetrachlorodibenzo-p-dioxin
Language	English
Dates of publication	2012-1015
Size	p. 39-47.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2012.05.006
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Zs.A 1127: Show issues

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Article ; Online: The aryl hydrocarbon receptor ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene regulate distinct genetic networks.

Swedenborg, Elin / Kotka, Maria / Seifert, Martin / Kanno, Jun / Pongratz, Ingemar / Rüegg, Joëlle

Molecular and cellular endocrinology

2012 Volume 362, Issue 1-2, Page(s) 39–47

Abstract	The two estrogen receptor isoforms ERα and ERβ mediate biological effects of estrogens, but are also targets for endocrine disruptive chemicals (EDCs), compounds that interfere with hormonal signaling. 3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling. However, in contrast to TCDD, 3-MC gives rise to metabolites with estrogenic properties. We compared gene expression profiles in HepG2 cells after exposure to 3-MC, TCDD, and the synthetic estrogen diethylstilbestrol (DES). Interestingly, we observed little overlap between the genetic networks activated by 3-MC and TCDD, two compounds sometimes considered as interchangeable AhR ligands. Like DES, 3-MC induced a number of ER-regulated genes and lead to recruitment of ERα to the promoters of such genes. Interestingly, in contrast to DES, the estrogenic effects exerted by 3-MC were exclusively observed in ERα, but not in ERβ-expressing cells, suggesting ER isoform selectivity of 3-MC-derived metabolites.
MeSH term(s)	Chromatin Immunoprecipitation ; Endocrine Disruptors/pharmacology ; Estrogen Receptor alpha/metabolism ; Gene Expression Regulation/drug effects ; Gene Regulatory Networks ; Genes ; Hep G2 Cells ; Humans ; Methylcholanthrene/pharmacology ; Oligonucleotide Array Sequence Analysis ; Polychlorinated Dibenzodioxins/pharmacology ; Promoter Regions, Genetic ; Protein Binding ; Real-Time Polymerase Chain Reaction ; Receptors, Aryl Hydrocarbon/agonists ; Transcriptional Activation/drug effects ; Transcriptome
Chemical Substances	Endocrine Disruptors ; Estrogen Receptor alpha ; Polychlorinated Dibenzodioxins ; Receptors, Aryl Hydrocarbon ; Methylcholanthrene (56-49-5)
Language	English
Publishing date	2012-10-15
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2012.05.006
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Zs.A 1127: Show issues

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Article: Regulation of estrogen receptor beta activity and implications in health and disease

Swedenborg, Elin / Power, Krista A / Cai, Wen / Pongratz, Ingemar / Rüegg, Joëlle

Cellular and molecular life sciences CMLS. 2009 Dec., v. 66, no. 24

2009

Abstract: Together with the estrogen receptor (ER) alpha, estrogen receptor beta (ERβ) mediates many of the physiological effects of estrogens. As ERβ is crucially involved in a variety of important physiological processes, its activity should be tightly regulated. ...

Abstract	Together with the estrogen receptor (ER) alpha, estrogen receptor beta (ERβ) mediates many of the physiological effects of estrogens. As ERβ is crucially involved in a variety of important physiological processes, its activity should be tightly regulated. ERβ regulation is achieved by hormone binding as well as by posttranslational modifications of the receptor. Furthermore, ERβ expression levels are under circadian control and can be regulated by DNA methylation of the ERβ promoter region. There are also a number of factors that can interfere with ERβ activity, such as phytoestrogens, endocrine disruptive chemicals, and growth factors. In this article, we outline different mechanisms of ERβ regulation and how they are implicated in various diseases. We also discuss how these insights might help to specifically target ERβ in drug design.
Language	English
Dates of publication	2009-12
Size	p. 3873-3894.
Publisher	SP Birkhäuser Verlag Basel
Publishing place	Basel
Document type	Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-009-0118-z
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Article ; Online: Regulation of estrogen receptor beta activity and implications in health and disease.

Swedenborg, Elin / Power, Krista A / Cai, Wen / Pongratz, Ingemar / Rüegg, Joëlle

Cellular and molecular life sciences : CMLS

2009 Volume 66, Issue 24, Page(s) 3873–3894

Abstract: Together with the estrogen receptor (ER) alpha, estrogen receptor beta (ER beta ) mediates many of the physiological effects of estrogens. As ER beta is crucially involved in a variety of important physiological processes, its activity should be tightly ... ...

Abstract	Together with the estrogen receptor (ER) alpha, estrogen receptor beta (ER beta ) mediates many of the physiological effects of estrogens. As ER beta is crucially involved in a variety of important physiological processes, its activity should be tightly regulated. ER beta regulation is achieved by hormone binding as well as by posttranslational modifications of the receptor. Furthermore, ER beta expression levels are under circadian control and can be regulated by DNA methylation of the ER beta promoter region. There are also a number of factors that can interfere with ER beta activity, such as phytoestrogens, endocrine disruptive chemicals, and growth factors. In this article, we outline different mechanisms of ER beta regulation and how they are implicated in various diseases. We also discuss how these insights might help to specifically target ER beta in drug design.
MeSH term(s)	Alternative Splicing ; DNA Methylation ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Models, Biological ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Phytoestrogens/metabolism ; Protein Binding ; Protein Processing, Post-Translational
Chemical Substances	Estrogen Receptor beta ; Phytoestrogens
Language	English
Publishing date	2009-08-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-009-0118-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 195: Show issues

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Article ; Online: Epigenetic regulation of glucose transporter 4 by estrogen receptor β.

Rüegg, Joëlle / Cai, Wen / Karimi, Mohsen / Kiss, Nimrod B / Swedenborg, Elin / Larsson, Catharina / Ekström, Tomas J / Pongratz, Ingemar

Molecular endocrinology (Baltimore, Md.)

2011 Volume 25, Issue 12, Page(s) 2017–2028

Abstract: Glucose transporter 4 (Glut4) is an important regulator of cellular glucose uptake in adipose tissue and skeletal muscle. The estrogen receptors α and β (ERα and ERβ) have been shown to regulate Glut4. However, the regulatory mechanisms are unclear, and ... ...

Abstract	Glucose transporter 4 (Glut4) is an important regulator of cellular glucose uptake in adipose tissue and skeletal muscle. The estrogen receptors α and β (ERα and ERβ) have been shown to regulate Glut4. However, the regulatory mechanisms are unclear, and there are conflicting results about the effects of the two ER isoforms on Glut4 activity. In this study we investigated how the lack of either ER isoform affects Glut4 expression in differentiated mouse embryonic fibroblasts. Our results demonstrate that Glut4 transcription is markedly reduced in cells lacking ERβ, both basally and upon induction by liver X receptor. These changes in Glut4 expression could not be explained by the lack of ERβ as ligand-activated transcription factor. They were rather brought about by hypermethylation of one single CpG in the Glut4 promoter in the ERβ-deficient cells. This CpG is part of an Sp1-binding site, and Sp1 binding was reduced by its methylation. Treatment with Sp1 inhibitor diminished Glut4 expression in wild-type, but not in ERβ-deficient cells, suggesting that reduced recruitment of Sp1 to the Glut4 promoter is responsible for the differences in Glut4 expression. Reintroduction of ERβ into ERβ-deficient cells partly restored Glut4 transcription and stabilized low DNA methylation after treatment with the DNA demethylating agent 5-Aza-2'-deoxycytidine. Our findings demonstrate the involvement of DNA methylation in Glut4 regulation and imply a novel function for ERβ in mediating epigenetic events and thereby regulating gene expression.
MeSH term(s)	Adipocytes/metabolism ; Animals ; Azacitidine/analogs & derivatives ; Azacitidine/pharmacology ; Cell Nucleus/metabolism ; Cells, Cultured ; CpG Islands ; DNA Methylation/drug effects ; DNA Modification Methylases/antagonists & inhibitors ; Decitabine ; Epigenesis, Genetic ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; Gene Knockout Techniques ; Glucose Transporter Type 4/genetics ; Glucose Transporter Type 4/metabolism ; Liver X Receptors ; Mice ; Orphan Nuclear Receptors/metabolism ; Promoter Regions, Genetic ; Protein Binding ; Protein Isoforms/metabolism ; Sp1 Transcription Factor/metabolism ; Transcription, Genetic
Chemical Substances	Estrogen Receptor alpha ; Estrogen Receptor beta ; Glucose Transporter Type 4 ; Liver X Receptors ; Orphan Nuclear Receptors ; Protein Isoforms ; Sp1 Transcription Factor ; Decitabine (776B62CQ27) ; DNA Modification Methylases (EC 2.1.1.-) ; Azacitidine (M801H13NRU)
Language	English
Publishing date	2011-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/me.2011-1054
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Zs.A 2261: Show issues

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Article: The transcription factor aryl hydrocarbon receptor nuclear translocator functions as an estrogen receptor beta-selective coactivator, and its recruitment to alternative pathways mediates antiestrogenic effects of dioxin.

Rüegg, Joëlle / Swedenborg, Elin / Wahlström, David / Escande, Aurelie / Balaguer, Patrick / Pettersson, Katarina / Pongratz, Ingemar

Molecular endocrinology (Baltimore, Md.)

2007 Volume 22, Issue 2, Page(s) 304–316

Abstract: The biological effects of dioxins are mediated by the aryl hydrocarbon receptor (AhR) and its dimerization partner, the AhR nuclear translocator (ARNT), and include interference with hormonal signaling pathways like the response to estrogens. The effects ...

Abstract	The biological effects of dioxins are mediated by the aryl hydrocarbon receptor (AhR) and its dimerization partner, the AhR nuclear translocator (ARNT), and include interference with hormonal signaling pathways like the response to estrogens. The effects of estrogens are mediated by two estrogen receptor (ER) isoforms, ERalpha and ERbeta, which belong to the family of nuclear receptors. We have previously shown that ARNT can act as coactivator of the ERs. In this study, we show that recruitment of ARNT to AhR or hypoxia-inducible factor-1alpha signaling pathways as well as small interfering RNA-mediated down-regulation of ARNT levels lead to a reduction in ER transcriptional activity. Using chromatin immunoprecipitation assays, we demonstrate that this decrease coincides with reduced recruitment of ARNT to estradiol-regulated promoters. We show further that coactivation by ARNT as well as inhibition by dioxin acts stronger on ERbeta than on ERalpha activity. Additionally, we demonstrate that the effects of ARNT are dependent on the A/B domain of the ERs with the A/B domain of ERbeta being considerably stronger in mediating the coactivating effects of ARNT. Taken together, our studies show that recruitment of ARNT to the AhR after dioxin treatment can account for the antiestrogenic effect of dioxins. Moreover, we show for the first time that the inhibitory effects of dioxin are more pronounced on ERbeta than on ERalpha.
MeSH term(s)	Animals ; Aryl Hydrocarbon Receptor Nuclear Translocator/genetics ; Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism ; Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Dimerization ; Dioxins/pharmacology ; Estradiol/pharmacology ; Estrogen Receptor alpha/chemistry ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor beta/chemistry ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Models, Biological ; Mutation ; Polychlorinated Dibenzodioxins/pharmacology ; Promoter Regions, Genetic/genetics ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Signal Transduction/drug effects ; Transcription, Genetic/drug effects
Chemical Substances	Dioxins ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Hypoxia-Inducible Factor 1, alpha Subunit ; Polychlorinated Dibenzodioxins ; Receptors, Aryl Hydrocarbon ; Aryl Hydrocarbon Receptor Nuclear Translocator (138391-32-9) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2007-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/me.2007-0128
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Zs.A 2261: Show issues

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Article ; Online: 3-Methylcholanthrene displays dual effects on estrogen receptor (ER) alpha and ER beta signaling in a cell-type specific fashion.

Swedenborg, Elin / Rüegg, Joëlle / Hillenweck, Anne / Rehnmark, Stefan / Faulds, Malin Hedengran / Zalko, Daniel / Pongratz, Ingemar / Pettersson, Katarina

Molecular pharmacology

2008 Volume 73, Issue 2, Page(s) 575–586

Abstract: The biological effects of 17beta-estradiol (E(2)) are mediated by the two estrogen receptor (ER) isoforms ERalpha and ERbeta. These receptors are ligand-inducible transcription factors that belong to the nuclear receptor superfamily. These receptors are ... ...

Abstract	The biological effects of 17beta-estradiol (E(2)) are mediated by the two estrogen receptor (ER) isoforms ERalpha and ERbeta. These receptors are ligand-inducible transcription factors that belong to the nuclear receptor superfamily. These receptors are also targets for a broad range of natural and synthetic compounds that induce ER activity, including dietary compounds, pharmaceuticals, and various types of environmental pollutants such as bisphenols and polychlorinated hydroxy-biphenyls. Here, we study the effect of the combustion byproduct 3-methylcholanthrene (3-MC) on ERalpha and ERbeta. 3-MC is a compound identified previously as an activator of the aryl hydrocarbon receptor (AhR). Activation of AhR is traditionally associated with an inhibition of the E(2) signaling network. In this study, we demonstrate that 3-MC is a cell-specific activator or inhibitor of E(2) signaling pathways. We show that 3-MC acts as a repressor in some cells, presumably via the AhR, whereas it is a potent activator of ER activity in other cells. It is interesting that we demonstrate that the estrogenic effects of 3-MC are dependent on the ability of cells to metabolize parental 3-MC to alternative compounds. In summary, our results suggest that exposure to AhR ligands like 3-MC can lead to either activation or repression of E(2) signaling, depending on the cellular context.
MeSH term(s)	Cell Line ; Cell Membrane/drug effects ; Cell Membrane/genetics ; Cell Membrane/metabolism ; Estradiol/metabolism ; Estradiol/physiology ; Estrogen Antagonists/pharmacology ; Estrogen Receptor alpha/biosynthesis ; Estrogen Receptor alpha/genetics ; Estrogen Receptor beta/biosynthesis ; Estrogen Receptor beta/genetics ; Humans ; Methylcholanthrene/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Transcription, Genetic/drug effects ; Transcription, Genetic/physiology
Chemical Substances	Estrogen Antagonists ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estradiol (4TI98Z838E) ; Methylcholanthrene (56-49-5)
Language	English
Publishing date	2008-02
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	124034-1
ISSN	1521-0111 ; 0026-895X
ISSN (online)	1521-0111
ISSN	0026-895X
DOI	10.1124/mol.107.036384
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Zs.A 525: Show issues

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Article: aryl hydrocarbon receptor ligands 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene regulate distinct genetic networks

Swedenborg, Elin / Kotka, Maria / Seifert, Martin / Kanno, Jun / Pongratz, Ingemar / Rüegg, Joëlle

Molecular and cellular endocrinology

Volume v. 362,, Issue no. 1

Abstract	The two estrogen receptor isoforms ERα and ERβ mediate biological effects of estrogens, but are also targets for endocrine disruptive chemicals (EDCs), compounds that interfere with hormonal signaling. 3-Methylcholanthrene (3-MC) and dioxin (TCDD) are EDCs and prototypical aryl hydrocarbon receptor (AhR) agonists, and can inhibit ER signaling. However, in contrast to TCDD, 3-MC gives rise to metabolites with estrogenic properties. We compared gene expression profiles in HepG2 cells after exposure to 3-MC, TCDD, and the synthetic estrogen diethylstilbestrol (DES). Interestingly, we observed little overlap between the genetic networks activated by 3-MC and TCDD, two compounds sometimes considered as interchangeable AhR ligands. Like DES, 3-MC induced a number of ER-regulated genes and lead to recruitment of ERα to the promoters of such genes. Interestingly, in contrast to DES, the estrogenic effects exerted by 3-MC were exclusively observed in ERα, but not in ERβ-expressing cells, suggesting ER isoform selectivity of 3-MC-derived metabolites.
Keywords	metabolites ; estrogenic properties ; estrogen receptors ; tetrachlorodibenzo-p-dioxin ; agonists ; genes ; human cell lines ; gene expression ; diethylstilbestrol
Language	English
Document type	Article
ISSN	0303-7207
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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