Ginecologia Clinical Gynecologic Endocrinology and

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Tamoxifen's agonistic ability is due to activation of TAF-1; its antagonistic activity is due to competitive inhibition of the estrogen-dependent activation of TAF-2. An estrogen-associated protein binds to the right hand side of TAF-2. Estrogen binding induces binding of this protein, which then activates transcription. This protein recognizes only an activated conformation of the estrogen receptor, the result of estrogen binding. Tamoxifen binding to the TAF-2 area does not activate this domain because, in at least one explanation, the conformational change does not allow binding of the estrogen-associated protein, the activating factor.

Heterogeneity of the hormone. Up- and down-regulation of receptors. Regulation of adenylate cyclase. Autocrine and Paracrine Regulation Factors Growth factors are polypeptides that modulate activity either in the cells in which they are produced or in nearby cells; hence, they are autocrine and paracrine regulators. Regulation factors of this type (yet another biologic family) are produced by local gene expression and protein translation, and they operate by binding to cell membrane receptors. The receptors usually contain an intracellular component with tyrosine kinase activity that is energized by a binding-induced conformational change that induces autophosphorylation.

105 The contact sites of estrogens and antiestrogens with the estrogen receptor are not identical. 106 When an antiestrogen binds to the estrogen receptor, the conformational changes that are induced alter the ability of the estrogen receptor-antiestrogen complex to modulate transcriptional activity. The relative agonist—antagonist activity is determined by the specific conformation achieved by the specific antiestrogen. Even though tamoxifen can block estrogen-stimulated transcription of many genes, its degree of antagonistic activity varies among different animals, different cell types, and with different promoters within single cells.

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