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Related Experiment Videos

RAC-3 is a NF-kappa B coactivator.

S Werbajh1, I Nojek, R Lanz

  • 1Deparmento de Cs. Biológicas, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón II, Argentina.

FEBS Letters
|November 30, 2000
PubMed
Summary

Nuclear receptor coactivator RAC3 modulates NF-kappa B activity, impacting cytokine and glucocorticoid signaling. Competition for RAC3 between glucocorticoid receptor (GR) and NF-kappa B offers a new mechanism for their functional antagonism.

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Area of Science:

  • Molecular biology
  • Cellular signaling
  • Gene transcription regulation

Background:

  • Cytokines and glucocorticoids exhibit mutual antagonism in cellular functions.
  • This antagonism is partly mediated by glucocorticoid receptor (GR)/nuclear factor-kappa B (NF-kappa B) transrepression.

Purpose of the Study:

  • To investigate the role of nuclear receptor coactivator RAC3 in modulating NF-kappa B transactivation.
  • To elucidate the mechanism of RAC3 in the context of GR/NF-kappa B cross-regulation.

Main Methods:

  • Investigated RAC3's interaction with the active form of NF-kappa B.
  • Assessed the effect of RAC3 overexpression on GR-dependent transcription under conditions of GR/NF-kappa B transrepression.

Main Results:

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  • RAC3 functions as a coactivator by directly binding to the active form of NF-kappa B.
  • Overexpression of RAC3 rescued GR-dependent transcription, overcoming the inhibitory effects of GR/NF-kappa B transrepression.

Conclusions:

  • RAC3 plays a crucial role in modulating NF-kappa B transactivation.
  • The competition between GR and NF-kappa B for binding to RAC3 represents a novel mechanism for their mutual functional antagonism.