[Reaction between dexamethasone-receptor complexes and isolated nuclei from Zajdela hepatoma and rat liver cells].
Temperature-activation of the hormone-receptor complex (HRC) was shown to be necessary to ensure its translocation from cytoplasm to nucleus both in the rat liver and hepatoma. Hepatoma nuclei bind 20 times less HRC derived from homologous hepatoma cytosol (0.15 pmol/mg DNA), but twice as much (5.6 pmol/mg DNA) of HRC from heterologous liver cytosol, as compared with the binding of HRC from normal liver cytosol by liver nuclei (3 pmol/mg DNA), Ka of HRC with the acceptor sites in hepatoma and liver nuclei were found to be practically of the same order of magnitude. The above findings suggest an inhibition of cytosol-nucleus translocation of HRC from the cytosol of hepatoma cells as a possible cause of the nonresponsiveness of the latter to the hormone.
D000818:Animals; D001665:Binding Sites; D002467:Cell Nucleus / Q000378:metabolism; D003600:Cytosol / Q000032:analysis; D003907:Dexamethasone / Q000378:metabolism*; D066298:In Vitro Techniques; D007700:Kinetics; D008099:Liver / Q000378:metabolism / Q000648:ultrastructure*; D008114:Liver Neoplasms, Experimental / Q000378:metabolism / Q000648:ultrastructure*; D008297:Male; D051381:Rats; D011956:Receptors, Cell Surface / Q000302:isolation & purification / Q000378:metabolism*
D011956:Receptors, Cell Surface; D003907:Dexamethasone
Vzaimodeĭstvie deksametazon-retseptornykh kompleksov s izolirovannymi iadrami iz kletok gepatomy Zaĭdela i pecheni krys.