Abstract
Membrane-initiated estrogen signaling is characterized by rapid onset of action and by relative insensitivity, at least in early stages, to inhibition of gene transcription or protein synthesis 1;2. These acute responses cannot be explained by traditional models of hormone action wherein steroid hormones act only as nuclear transcription factors. The latter nuclear-initiated mechanism requires binding of estradiol to its cognate nuclear receptor, followed by receptor dimerization and binding with specific estrogen-responsive elements (ERE) in DNA, leading to the later regulation of gene transcription and promotion of cell growth. Nonetheless, integration of nuclear- and membrane-initiated signaling by estrogens likely contributes to the full biologic effects of hormone.
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