RAC‐3 is a NF‐κB coactivator

Autores
Werbajh, Santiago Enrique; Nojek Barbieri, Ignacio Martin; Lanz, Rainer; Costas, Monica Alejandra
Año de publicación
2000
Idioma
español castellano
Tipo de recurso
artículo
Estado
versión publicada
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.
Fil: Werbajh, Santiago Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiología, Biología Molecular y Celular. Laboratorio de Fisiología y Biología Molecular; Argentina
Fil: Nojek Barbieri, Ignacio Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Lanz, Rainer. Baylor College of Medicine; Estados Unidos
Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/101409

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spelling RAC‐3 is a NF‐κB coactivatorWerbajh, Santiago EnriqueNojek Barbieri, Ignacio MartinLanz, RainerCostas, Monica Alejandrahttps://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3It 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.Fil: Werbajh, Santiago Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiología, Biología Molecular y Celular. Laboratorio de Fisiología y Biología Molecular; ArgentinaFil: Nojek Barbieri, Ignacio Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Lanz, Rainer. Baylor College of Medicine; Estados UnidosFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaWiley2000-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/101409Werbajh, Santiago Enrique; Nojek Barbieri, Ignacio Martin; Lanz, Rainer; Costas, Monica Alejandra; RAC‐3 is a NF‐κB coactivator; Wiley; FEBS Letters; 485; 2-3; 12-2000; 195-1990014-5793CONICET DigitalCONICETspainfo:eu-repo/semantics/altIdentifier/url/https://febs.onlinelibrary.wiley.com/doi/full/10.1016/S0014-5793%2800%2902223-7info:eu-repo/semantics/altIdentifier/doi/10.1016/S0014-5793%2800%2902223-7info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:24:47Zoai:ri.conicet.gov.ar:11336/101409instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:24:47.484CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv RAC‐3 is a NF‐κB coactivator
title RAC‐3 is a NF‐κB coactivator
spellingShingle RAC‐3 is a NF‐κB coactivator
Werbajh, Santiago Enrique
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
dc.creator.none.fl_str_mv Werbajh, Santiago Enrique
Nojek Barbieri, Ignacio Martin
Lanz, Rainer
Costas, Monica Alejandra
author Werbajh, Santiago Enrique
author_facet Werbajh, Santiago Enrique
Nojek Barbieri, Ignacio Martin
Lanz, Rainer
Costas, Monica Alejandra
author_role author
author2 Nojek Barbieri, Ignacio Martin
Lanz, Rainer
Costas, Monica Alejandra
author2_role author
author
author
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.5
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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.
Fil: Werbajh, Santiago Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiología, Biología Molecular y Celular. Laboratorio de Fisiología y Biología Molecular; Argentina
Fil: Nojek Barbieri, Ignacio Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Lanz, Rainer. Baylor College of Medicine; Estados Unidos
Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
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.
publishDate 2000
dc.date.none.fl_str_mv 2000-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/101409
Werbajh, Santiago Enrique; Nojek Barbieri, Ignacio Martin; Lanz, Rainer; Costas, Monica Alejandra; RAC‐3 is a NF‐κB coactivator; Wiley; FEBS Letters; 485; 2-3; 12-2000; 195-199
0014-5793
CONICET Digital
CONICET
url http://hdl.handle.net/11336/101409
identifier_str_mv Werbajh, Santiago Enrique; Nojek Barbieri, Ignacio Martin; Lanz, Rainer; Costas, Monica Alejandra; RAC‐3 is a NF‐κB coactivator; Wiley; FEBS Letters; 485; 2-3; 12-2000; 195-199
0014-5793
CONICET Digital
CONICET
dc.language.none.fl_str_mv spa
language spa
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info:eu-repo/semantics/altIdentifier/doi/10.1016/S0014-5793%2800%2902223-7
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
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dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
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