Estrogen-Induced Growth of Uterine Cells

Evidence for Involvement of Surface Membranes, Calcium, and Proteinase Activity
  • Richard J. Pietras
  • Clara M. Szego
Part of the Biochemical Endocrinology book series (BIOEND)


A general hypothesis has been developed in recent years to describe the mechanism of action of steriod hormones. Circulating steroid, having dissociated from serum carrier proteins, is considered to diffuse passively into most tissue cells (Peck et al., 1973; Gorski and Gannon, 1976). The hormones are retained and accumulated only in responsive cells by interactions with extranuclear macromolecules that possess high affinity and specificity for hormone (Jensen and Jacobson, 1962; Talwar et al., 1964; Gorski et al., 1968; Jensen et al., 1974; King and Mainwaring, 1974). In the chick, labeled hormone is detected bound to its receptor in the oviduct within 1-2 min following injection (O’Malley et al., 1970). Once bound to hormone, the receptor is transformed or activated (Jensen et al., 1968; Puca et al., 1972) and thereby rendered capable, within 2-4 min after injection (O’Malley et al., 1970), of transport to the nucleus. Within the nucleus, the steroid—receptor complex interacts with unspecified “acceptor sites” in the chromosomal material and thereby elicits the synthesis of specific RNA species that are believed to underlie expression of the phenotypic effects (Hamilton, 1968; Gorski and Gannon, 1976; Buller and O’Malley, 1976; Thrall et al., 1978).


Cationic Liposome Endometrial Cell Chemically Define Medium Estradiol Receptor Cytosol Receptor 
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Copyright information

© Plenum Press, New York 1981

Authors and Affiliations

  • Richard J. Pietras
    • 1
  • Clara M. Szego
    • 1
  1. 1.Department of Biology and the Molecular Biology InstituteUniversity of CaliforniaLos AngelesUSA

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