The ER/AP1 Pathway: A Window on the Cell-Specific Estrogen-like Effects of Antiestrogens
We study an unusual pathway of estrogen receptor (ER) action, in which ER indirectly alters the transactivation capacity of the jun/fos complex (AP1 proteins), rather than stimulating gene expression by directly binding DNA. Here, we review the rationale for studying this pathway and the reasons for thinking that elucidation of ER/AP1 interactions will help us design the next generation of antiestrogens and hormone replacement therapies.
KeywordsEstrogen Receptor MCF7 Cell Estrogen Response Element Ishikawa Cell Antiestrogen Action
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