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Significance The antiinflammatory property of natural glucocorticoids (GCs) was demonstrated more than 60 years ago. Since then, synthetic GCs have been widely used to combat inflammatory and allergic disorders. However, multiple severe undesirable side effects associated with long-term GC treatments, as well as induction of glucocorticoid resistance associated with such treatments, limit their therapeutic usefulness. In the present study, we unveiled the molecular mechanism underlying the GC-induced GC receptor (GR)-mediated tethered indirect transrepression. This knowledge paves the way to the future educated design and screening of drugs, collectively named selective GR agonists, which would exhibit the major therapeutically beneficial properties of GCs, but would be devoid of undesirable debilitating effects upon prolonged GC therapy.

Glucocorticoid-induced tethered transrepression requires SUMOylation of GR and formation of a SUMO-SMRT/NCoR1-HDAC3 repressing complex