Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 290, Issue 1-2, Pages 24-30Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2008.04.003
Keywords
estrogen receptor alpha; estrogen response element; non-classical signaling; negative feedback; sexual behavior
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Funding
- NICHD NIH HHS [U54 HD041859-01A10003, U54 HD041859, T32 HD007068-30, R01 HD020677-17, T32 HD007068, R01 HD020677] Funding Source: Medline
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Estrogen receptor alpha (ER alpha) mediates estrogen (E2) actions in the brain and is critical for normal reproductive function and behavior. In the classical pathway, ER alpha binds to estrogen response elements (EREs) to regulate gene transcription. ER alpha can also participate in several non-classical pathways, including ERE-independent gene transcription via protein-protein interactions with transcription factors and rapid, non-genotropic pathways. To distinguish between ERE-dependent and ERE-independent mechanisms of E2 action in vivo, we have created ER alpha null mice that possess an ER knock-in Mutation (E207A/G208A; AA), in which the mutant ER alpha cannot bind to DNA but retains activity in ERE-independent pathways (ER alpha(-/AA) mice). Understanding the molecular mechanisms of ER alpha action will be helpful in developing pharmacological therapies that differentiate between ERE-dependent and ERE-independent processes. This review focuses on how the ER alpha(-/AA) model has contributed to our knowledge of ER alpha signaling mechanisms in estrogen regulation of the reproductive axis and sexual behavior. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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