RAC‐3 is a NF‐κB coactivator

Abstract

It has been shown that the molecular mechanism by which cytokines and glucocorticoids mutually antagonize their functions involves a mutual glucocorticoid receptor (GR)/nuclear factor‐κB (NF‐κB) transrepression. Here we report a role for the nuclear receptor coactivator RAC3, in modulating NF‐κB transactivation. We found that RAC3 functions as a coactivator by binding to the active form of NF‐κB and that overexpression of RAC3 restores GR‐dependent transcription neglecting GR/NF‐κB transrepression. The competition between GR and NF‐κB for binding to RAC3 may represent a general mechanism by which both transcription factors mutually antagonize their activity.