RAC-3 is a NF-κB coactivator

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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...

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Autores principales:	Werbajh, S., Nojek, I., Lanz, R., Costas, M.A.
Formato:	JOUR
Materias:	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
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_00145793_v485_n2-3_p195_Werbajh
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	todo:paper_00145793_v485_n2-3_p195_Werbajh
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spelling	todo:paper_00145793_v485_n2-3_p195_Werbajh2023-10-03T14:13:06Z RAC-3 is a NF-κB coactivator Werbajh, S. Nojek, I. Lanz, R. Costas, M.A. 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 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. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00145793_v485_n2-3_p195_Werbajh
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	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
spellingShingle	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 Werbajh, S. Nojek, I. Lanz, R. Costas, M.A. RAC-3 is a NF-κB coactivator
topic_facet	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
description	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.
format	JOUR
author	Werbajh, S. Nojek, I. Lanz, R. Costas, M.A.
author_facet	Werbajh, S. Nojek, I. Lanz, R. Costas, M.A.
author_sort	Werbajh, S.
title	RAC-3 is a NF-κB coactivator
title_short	RAC-3 is a NF-κB coactivator
title_full	RAC-3 is a NF-κB coactivator
title_fullStr	RAC-3 is a NF-κB coactivator
title_full_unstemmed	RAC-3 is a NF-κB coactivator
title_sort	rac-3 is a nf-κb coactivator
url	http://hdl.handle.net/20.500.12110/paper_00145793_v485_n2-3_p195_Werbajh
work_keys_str_mv	AT werbajhs rac3isanfkbcoactivator AT nojeki rac3isanfkbcoactivator AT lanzr rac3isanfkbcoactivator AT costasma rac3isanfkbcoactivator
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RAC-3 is a NF-κB coactivator

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