RAC-3 is a NF-κB coactivator

En:

FEBS Lett. 2000;485(2-3):195-199

Fecha:

2000

Formato:

application/pdf

Tipo de documento:

info:eu-repo/semantics/article
info:ar-repo/semantics/artículo
info:eu-repo/semantics/publishedVersion

Descriptores:

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

Descripción:

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.

Identificador(es):

http://hdl.handle.net/20.500.12110/paper_00145793_v485_n2-3_p195_Werbajh

Derechos:

info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/2.5/ar