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: Artículo publishedVersion
Lenguaje:Inglés
Publicado: 2000
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
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spelling paperaa:paper_00145793_v485_n2-3_p195_Werbajh2023-06-12T16:41:49Z RAC-3 is a NF-κB coactivator FEBS Lett. 2000;485(2-3):195-199 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. 2000 info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion application/pdf eng 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)
language Inglés
orig_language_str_mv eng
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 Artículo
Artículo
publishedVersion
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
publishDate 2000
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
_version_ 1769810263795564544

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