Type II Binding Sites: Cellular Origin and an Endogenous Ligand

Abstract

Previous studies from our laboratory have described two specific nuclear estrogen-binding sites in normal (Eriksson et al., 1978; Clark et al., 1978; Markaverich and Clark, 1979; Watson and Clark, 1980) and malignanttissues. Type I sites represent the classical estrogen receptor, which has a high affinity for estradiol (K _k = 0.1 − 1.0 nM) and is present in target tissues in relatively low quantities. Nuclear type II sites appear to be a specific nuclear response to estrogenic hormones that is highly correlated with uterine hypertrophy and hyperplasia (Markaverich et al., 1981a,b,c). Likewise, nuclear type II sites are elevated in neoplastic tissues such as mouse mammary tumors (Watson et al., 1977; Watson and Clark, 1980; Watson et al., 1981) and human breast cancer (Syne et al., 1982).