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

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.

Epigenetic regulation of glucose transporter 4 by estrogen receptor β.

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.

Endocrine disruptors targeting ERbeta function.

Endocrine disruptive chemicals (EDCs) circulating in the environment constitute a risk to ecosystems, wildlife and human health. Oestrogen receptor (ER) alpha and beta are targeted by various kinds of EDCs but the molecular mechanisms and long-term consequences of exposure are largely unknown. Some biological effects of EDCs are mediated by the aryl hydrocarbon receptor (AhR), which is a key player in the cellular defence against xenobiotic substances.

AhR and ARNT modulate ER signaling.

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.

Regulation of estrogen receptor beta activity and implications in health and disease.

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.

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

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.

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

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.

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.

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.