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

• Published in: Cellular and molecular life sciences : CMLS Vol. 66; no. 24; pp. 3873 - 3894
• Main Authors: Swedenborg, Elin, Power, Krista A, Cai, Wen, Pongratz, Ingemar, Rüegg, Joëlle
• Format: Journal Article
• Language: English
• Published: Basel Basel : SP Birkhäuser Verlag Basel 01-12-2009; SP Birkhäuser Verlag Basel; Springer Nature B.V
• Subjects: Alternative Splicing; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cancer; Cell Biology; Diabetes; DNA Methylation; Endocrine disruptors; Endocrine system; Estrogen Receptor beta - genetics; Estrogen Receptor beta - metabolism; Estrogens; Gene Expression Regulation, Neoplastic; Growth factors; Humans; Life Sciences; Medicin och hälsovetenskap; Models, Biological; Neoplasms - genetics; Neoplasms - metabolism; Neoplasms - pathology; Physiology; Phytoestrogens - metabolism; Protein Binding; Protein Processing, Post-Translational; Review; Phytoestrogens; Endocrine disruption; Circadian regulation; DNA methylation; Estrogen receptor beta; Cancer; Diabetes type 2
• ISSN: 1420-682X; 1420-9071; 1420-9071
• DOI: 10.1007/s00018-009-0118-z

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.