CU Molecular, Cellular, and Developmental Biology
MCDB Home > Postdoctoral > PostDocPublications > NojekIMPublications > RAC-3 is a NF-kappa B coactivator
Document Actions

RAC-3 is a NF-kappa B coactivator


RAC-3 is a NF-kappa B coactivator

7350

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.


Werbajh S, Nojek I, Lanz R, Costas MA

FEBS letters

2000-11-24 00:00

485

2

195-9

Binding, Competitive,Glucocorticoids,Hela Cells,Humans,Immunosorbent Techniques,NF-kappa B,Receptors, Glucocorticoid,Response Elements,Trans-Activators,Transcription Factor RelA,Transcription Factors,Transcription, Genetic,Transfection,Tumor Necrosis Factor-alpha,Glucocorticoids,NF-kappa B,Receptors, Glucocorticoid,Trans-Activators,Transcription Factor RelA,Transcription Factors,Tumor Necrosis Factor-alpha,steroid receptor coactivator AIB1

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

FEBS Lett.


0014-5793


S0014-5793(00)02223-7


0

False

11094166

Ignacio Nojek
University of Colorado Contact Us  |   Legal & Trademarks  |  Privacy