Absence in Glucocorticoid-resistant Mouse Lymphoma P1798 of a Glucocorticoid Receptor Domain Responsible for Biological Effects

摘要: Abstract Glucocorticoid-resistant (CR), in contrast to glucocorticoid-sensitive (CS), mouse lymphoma P1798 was shown lack antiglucocorticoid receptor immunoactivity. Antibodies raised against the purified rat liver glucocorticoid (GR) cross-reacted with GR from CS, but not CR, lymphoma. Using highly specific antisera an indirect competitive enzyme-linked immunosorbent assay, it demonstrated that α-chymotrypsin digestion of CS caused a separation “resistant-like” nonimmunogenic steroid and DNA-binding domain (Stockes9 radius, 3.3 nm) immunoactive (Stokes9 2.6 nm). In lymphoma, neither before nor after digestion, immunoactivity could be found cytosol CR This assayed chromatography on DNA-cellulose or gel filtration Agarose A (0.5 m). These results suggest containing determinant(s), normally removed by limited proteolysis α-chymotrypsin, appears missing cytosol. It seems this plays important role mechanism action glucocorticoids. might mutation has occurred affecting genome resulting defective transcription gene(s)