Non-classical genomic estrogen receptor (ER)/specificity protein and ER/activating protein-1 signaling pathways. Academic Article

abstract

• 17beta-estradiol binds to the estrogen receptor (ER) to activate gene expression or repression and this involves both genomic (nuclear) and non-genomic (extranuclear) pathways. Genomic pathways include the classical interactions of ligand-bound ER dimers with estrogen-responsive elements in target gene promoters. ER-dependent activation of gene expression also involves DNA-bound ER that subsequently interacts with other DNA-bound transcriptions factors and direct ER-transcription factor (protein-protein) interactions where ER does not bind promoter DNA. Ligand-induced activation of ER/specificity protein (Sp) and ER/activating protein-1 [(AP-1); consisting of jun/fos] complexes are important pathways for modulating expression of a large number of genes. This review summarizes some of the characteristics of ER/Sp- and ER/AP-1-mediated transactivation, which are dependent on ligand structure, cell context, ER-subtype (ERalpha and ERbeta), and Sp protein (SP1, SP3, and SP4) and demonstrates that this non-classical genomic pathway is also functional in vivo.

authors

• Safe, Stephen

published proceedings

• J Mol Endocrinol

author list (cited authors)

• Safe, S., & Kim, K.

citation count

• 256

complete list of authors

• Safe, Stephen||Kim, Kyounghyun

publication date

• November 2008

publisher

• Bioscientifica  Publisher

published in

• Journal of Molecular Endocrinology  Journal

keywords

• Animals
• Cell Line, Tumor
• Estradiol
• Gene Expression Regulation
• Humans
• Ligands
• Receptors, Estrogen
• Signal Transduction
• Sp1 Transcription Factor
• Transcription Factor AP-1

Digital Object Identifier (DOI)

• 10.1677/JME-08-0103

start page

• 263

end page

• 275

volume

• 41

issue

• 5

URL

• http://dx.doi.org/10.1677/jme-08-0103