Abstract
The model for estrogen action proposed by Jensen & Gorski more than twenty years ago has served as a unifying theory to explain regulation of gene expression by many steroid hormones (34, 48). Each hormone triggers an allosteric change in a specific receptor protein converting it from a low affinity DNA-binding state to one with relatively higher affinity for DNA elements in the vicinities of target genes. This tighter DNA binding interac tion is thought to catalyze the assembly of transcriptional complexes at nearby sites and activate target cell gene expression (111). Despite extensive characterization of the receptor proteins and their target DNA sequences, our knowledge of how the activated receptor initiates transcription from hormone responsive genes is still incomplete (for other reviews see 5, 14, 24). Recent identification of several steroid hormone receptor genes has helped to uncover a large family of nuclear receptor or ligand-dependent transcription
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