Specific binding of estrogen receptor to the estrogen response element.

Abstract

Gene transfer studies have shown that estrogen regulation of specific genes is mediated by estrogen response elements (ERE). We report that binding of the estrogen receptor to the ERE can be detected by a gel retardation (band shift) assay. This binding interaction was highly sequence and receptor specific. Methylation interference analysis showed that the ERE contact sites of estrogen receptor displayed a perfect twofold rotational symmetry. This is compatible with estrogen receptor binding to the ERE as a head-to-head dimer.

Retinoic acid receptor expression vector inhibits differentiation of F9 embryonal carcinoma cells.

“…Three distinct and testable possibilities might explain the mechanism: (1) The SAC RAR-CB protein cannot transcriptionally activate retinoic acid-inducible or -repressible genes but can compete effectively for mRAR DNAbinding sites; (2) the mRAR(s) must dimerize to functionally bind to specific DNA-binding sites [as has been suggested for steroid hormone receptors (Kumar and Chambon 1988;Tsai et al 1988;Klein-Hitpass et al 1989)], and the SAC RAR-CB fusion protein is dimerizing with endogenous receptors and functionally inactivating them; or (3) the overexpression of the A/B domain of the SAC RAR-CB fusion protein is competing for factors required for the proper functioning of endogenous mRAR(s) [as has been suggested for the A/B domain of the estrogen receptor (Meyer et al 1989)]. These possibilities can be examined through a combination of domain mapping of the SAC RAR-CB vector to identify what sequences are necessary for this dominant-negative effect, and through in vitro DNA-binding studies with the hRAR-alpha and SAC RAR-CB fusion proteins.…”

Identification of Estrogen-Responsive Genes in Neuroblastoma SK-ER3 Cells

“…Estrogens regulate gene transcription by binding through their cognate receptors to specific regulatory DNA sequences within the promoter of target genes (Evans, 1988;Kumar and Chambon, 1988;Klein-Hitpass et al, 1989). Conceptually, the same molecular mechanisms should be used by estrogens in neural cells.…”

Pleiotropic actions of estrogen: a mitochondrial matter

“…Estrogen-activated ERs bind either to estrogen response elements or to other DNA-binding proteins located at promoters of estrogen-regulated genes (35,54). This interaction facilitates recruitment of specific coactivators and chromatin remodeling enzymes, capable of influencing the tran-scriptional machinery complex; hence, regulating gene expression (40).…”