'Activation-labile' glucocorticoid-receptor complexes of a steroid-resistant variant of CEM-C7 human lymphoid cells.
For cytoplasmic glucocorticoid-receptor complexes to enter and accumulate in the nucleus a temperature-dependent event, 'activation' is required. Activation can be achieved in vitro by increased ionic strength, dilution or gel filtration and is manifested by an increased affinity of steroid-receptor complex for DNA and an altered elution profile from ion-exchange resins. Munck and Foley have shown that activated complexes isolated from thymocytes elute from DEAE-cellulose in a manner identical to complexes activated in vitro. We report here that DEAE-cellulose chromatography of steroid-receptor complexes from CEM-C7, a cloned human leukaemic T-cell line sensitive to the cytolytic action of glucocorticoids, and its steroid-resistant subclone 4R4 demonstrated that steroid receptors of clone 4R4 cannot form stable activated complexes. This defines a new defect in receptor action, activation lability (r+act1), which is unlike either the r-, r+nt-, or r+nti phenotypes previously described for mouse lymphoid variants.
D000818:Animals; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D002843:Chromatin / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism; D006801:Humans; D007942:Leukemia, Experimental / Q000378:metabolism*; D008982:Molybdenum / Q000494:pharmacology; D009154:Mutation; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000235:genetics*; D011987:Receptors, Steroid / Q000235:genetics*; D013601:T-Lymphocytes / Q000378:metabolism; D014222:Triamcinolone Acetonide / Q000378:metabolism
D002843:Chromatin; D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D003907:Dexamethasone; D008982:Molybdenum; D014222:Triamcinolone Acetonide