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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/101409
Ver los metadatos del registro completo
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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/url/https://febs.onlinelibrary.wiley.com/doi/full/10.1016/S0014-5793%2800%2902223-7 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/ |
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openAccess |
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https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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Wiley |
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Wiley |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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