RAC-3 is a NF-κB coactivator

• Autores: Werbajh, S.; Nojek, I.; Lanz, R.; Costas, M.A.
• Año de publicación: 2000
• Idioma: inglés
• Tipo de recurso: artículo
• Fuente: FEBS Lett. 2000;485(2-3):195-199
• Materia: Glucocorticoid receptor; Nuclear factor-κB; Nuclear receptor coactivator; Tumor necrosis factor; glucocorticoid receptor; immunoglobulin enhancer binding protein; transcription factor; transcription factor rac 3; tumor necrosis factor; unclassified drug; article; competitive inhibition; genetic transfection; human; human cell; modulation; molecular biology; priority journal; protein analysis; protein binding; protein expression; transactivation; transcription regulation; 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
• Institución: Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales

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. (C) 2000 Federation of European Biochemical Societies.
Fil:Nojek, I. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Costas, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.