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'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.[1]References
- 'Activation-labile' glucocorticoid-receptor complexes of a steroid-resistant variant of CEM-C7 human lymphoid cells. Schmidt, T.J., Harmon, J.M., Thompson, E.B. Nature (1980) [Pubmed]
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