RAC-3 is a NF-κB coactivator
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 tra...
| Autores: | , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2000 |
| País: | Argentina |
| Institución: | Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
| Repositorio: | Biblioteca Digital (UBA-FCEN) |
| Idioma: | inglés |
| OAI Identifier: | paperaa:paper_00145793_v485_n2-3_p195_Werbajh |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_00145793_v485_n2-3_p195_Werbajh |
| Access Level: | acceso abierto |
| Palabra clave: | 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 |
| Sumario: | 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. |
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