RAC-3 is a NF-kappa B coactivator

FEBS Lett. 2000 Nov 24;485(2-3):195-9. doi: 10.1016/s0014-5793(00)02223-7.

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-kappa B (NF-kappa B) transrepression. Here we report a role for the nuclear receptor coactivator RAC3, in modulating NF-kappa B transactivation. We found that RAC3 functions as a coactivator by binding to the active form of NF-kappa B and that overexpression of RAC3 restores GR-dependent transcription neglecting GR/NF-kappa B transrepression. The competition between GR and NF-kappa B for binding to RAC3 may represent a general mechanism by which both transcription factors mutually antagonize their activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Binding, Competitive
  • Glucocorticoids / pharmacology
  • HeLa Cells
  • Humans
  • Immunosorbent Techniques
  • NF-kappa B / analysis
  • NF-kappa B / metabolism*
  • Nuclear Receptor Coactivator 3
  • Receptors, Glucocorticoid / metabolism*
  • Response Elements
  • Trans-Activators / genetics
  • Trans-Activators / metabolism
  • Trans-Activators / pharmacology*
  • Transcription Factor RelA
  • Transcription Factors*
  • Transcription, Genetic
  • Transfection
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Glucocorticoids
  • NF-kappa B
  • Receptors, Glucocorticoid
  • Trans-Activators
  • Transcription Factor RelA
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Nuclear Receptor Coactivator 3