The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action
- Autores
- Colo, Georgina Pamela; Rubio, María Fernanda; Nojek Barbieri, Ignacio Martin; Werbajh, Santiago Enrique; Echeverria, Pablo Christian; Alvarado, Cecilia Viviana; Nahmod, Victor Elias; Galigniana, Mario Daniel; Costas, Monica Alejandra
- Año de publicación
- 2007
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The p160 nuclear receptor coactivators represent a family of molecules, which are recruited by steroid nuclear receptors as well as other transcription factors that are over-expressed in several tumors. We investigated the role of one member of this family on the sensitivity of cells to apoptosis. We observed that over-expression of the RAC3 p160 coactivator inhibits hydrogen peroxide-induced cell death in HEK293 cells. The mechanism involves the activation of anti-apoptotic pathways mediated through enhanced NF-kB activity, inhibition of caspase-9 activation, diminished AIF nuclear localization and the change in the activation pattern of several kinases, including the increase in both AKT and p38 kinases activities, and inhibition of ERK2. Moreover, RAC3 has been found associated to a protein complex containing AIF, Hsp90 and dynein, suggesting a role for the coactivator in the cytoplasmatic-nuclear-transport of these proteins associated to cytoskeleton. These results demonstrate that there are several molecular pathways that could be affected by their over-expression, including those not restricted to steroid regulation or the nuclear action of coactivators, which results in diminished sensitivity to apoptosis. Furthermore, this could represent one mechanism by which coactivators contribute to tumor development.
Fil: Colo, Georgina Pamela. 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: Rubio, María Fernanda. 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: 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: Werbajh, Santiago Enrique. 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: Echeverria, Pablo Christian. 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: Alvarado, Cecilia Viviana. 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: Nahmod, Victor Elias. 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: Galigniana, Mario Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
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 - Materia
-
APOPTOSIS
RAC3
COACTIVADORES
NF-KB - 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:11336/104934
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The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic actionColo, Georgina PamelaRubio, María FernandaNojek Barbieri, Ignacio MartinWerbajh, Santiago EnriqueEcheverria, Pablo ChristianAlvarado, Cecilia VivianaNahmod, Victor EliasGaligniana, Mario DanielCostas, Monica AlejandraAPOPTOSISRAC3COACTIVADORESNF-KBhttps://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3The p160 nuclear receptor coactivators represent a family of molecules, which are recruited by steroid nuclear receptors as well as other transcription factors that are over-expressed in several tumors. We investigated the role of one member of this family on the sensitivity of cells to apoptosis. We observed that over-expression of the RAC3 p160 coactivator inhibits hydrogen peroxide-induced cell death in HEK293 cells. The mechanism involves the activation of anti-apoptotic pathways mediated through enhanced NF-kB activity, inhibition of caspase-9 activation, diminished AIF nuclear localization and the change in the activation pattern of several kinases, including the increase in both AKT and p38 kinases activities, and inhibition of ERK2. Moreover, RAC3 has been found associated to a protein complex containing AIF, Hsp90 and dynein, suggesting a role for the coactivator in the cytoplasmatic-nuclear-transport of these proteins associated to cytoskeleton. These results demonstrate that there are several molecular pathways that could be affected by their over-expression, including those not restricted to steroid regulation or the nuclear action of coactivators, which results in diminished sensitivity to apoptosis. Furthermore, this could represent one mechanism by which coactivators contribute to tumor development.Fil: Colo, Georgina Pamela. 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: Rubio, María Fernanda. 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: 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: Werbajh, Santiago Enrique. 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: Echeverria, Pablo Christian. 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: Alvarado, Cecilia Viviana. 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: Nahmod, Victor Elias. 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: Galigniana, Mario Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: 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; ArgentinaNature Publishing Group2007-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/104934Colo, Georgina Pamela; Rubio, María Fernanda; Nojek Barbieri, Ignacio Martin; Werbajh, Santiago Enrique; Echeverria, Pablo Christian; et al.; The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action; Nature Publishing Group; Oncogene; 27; 17; 10-2007; 2430-24440950-9232CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/1210900info:eu-repo/semantics/altIdentifier/doi/10.1038/sj.onc.1210900info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:58:45Zoai:ri.conicet.gov.ar:11336/104934instacron: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:34982025-09-03 09:58:45.821CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
title |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
spellingShingle |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action Colo, Georgina Pamela APOPTOSIS RAC3 COACTIVADORES NF-KB |
title_short |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
title_full |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
title_fullStr |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
title_full_unstemmed |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
title_sort |
The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action |
dc.creator.none.fl_str_mv |
Colo, Georgina Pamela Rubio, María Fernanda Nojek Barbieri, Ignacio Martin Werbajh, Santiago Enrique Echeverria, Pablo Christian Alvarado, Cecilia Viviana Nahmod, Victor Elias Galigniana, Mario Daniel Costas, Monica Alejandra |
author |
Colo, Georgina Pamela |
author_facet |
Colo, Georgina Pamela Rubio, María Fernanda Nojek Barbieri, Ignacio Martin Werbajh, Santiago Enrique Echeverria, Pablo Christian Alvarado, Cecilia Viviana Nahmod, Victor Elias Galigniana, Mario Daniel Costas, Monica Alejandra |
author_role |
author |
author2 |
Rubio, María Fernanda Nojek Barbieri, Ignacio Martin Werbajh, Santiago Enrique Echeverria, Pablo Christian Alvarado, Cecilia Viviana Nahmod, Victor Elias Galigniana, Mario Daniel Costas, Monica Alejandra |
author2_role |
author author author author author author author author |
dc.subject.none.fl_str_mv |
APOPTOSIS RAC3 COACTIVADORES NF-KB |
topic |
APOPTOSIS RAC3 COACTIVADORES NF-KB |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.5 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
The p160 nuclear receptor coactivators represent a family of molecules, which are recruited by steroid nuclear receptors as well as other transcription factors that are over-expressed in several tumors. We investigated the role of one member of this family on the sensitivity of cells to apoptosis. We observed that over-expression of the RAC3 p160 coactivator inhibits hydrogen peroxide-induced cell death in HEK293 cells. The mechanism involves the activation of anti-apoptotic pathways mediated through enhanced NF-kB activity, inhibition of caspase-9 activation, diminished AIF nuclear localization and the change in the activation pattern of several kinases, including the increase in both AKT and p38 kinases activities, and inhibition of ERK2. Moreover, RAC3 has been found associated to a protein complex containing AIF, Hsp90 and dynein, suggesting a role for the coactivator in the cytoplasmatic-nuclear-transport of these proteins associated to cytoskeleton. These results demonstrate that there are several molecular pathways that could be affected by their over-expression, including those not restricted to steroid regulation or the nuclear action of coactivators, which results in diminished sensitivity to apoptosis. Furthermore, this could represent one mechanism by which coactivators contribute to tumor development. Fil: Colo, Georgina Pamela. 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: Rubio, María Fernanda. 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: 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: Werbajh, Santiago Enrique. 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: Echeverria, Pablo Christian. 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: Alvarado, Cecilia Viviana. 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: Nahmod, Victor Elias. 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: Galigniana, Mario Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina 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 |
The p160 nuclear receptor coactivators represent a family of molecules, which are recruited by steroid nuclear receptors as well as other transcription factors that are over-expressed in several tumors. We investigated the role of one member of this family on the sensitivity of cells to apoptosis. We observed that over-expression of the RAC3 p160 coactivator inhibits hydrogen peroxide-induced cell death in HEK293 cells. The mechanism involves the activation of anti-apoptotic pathways mediated through enhanced NF-kB activity, inhibition of caspase-9 activation, diminished AIF nuclear localization and the change in the activation pattern of several kinases, including the increase in both AKT and p38 kinases activities, and inhibition of ERK2. Moreover, RAC3 has been found associated to a protein complex containing AIF, Hsp90 and dynein, suggesting a role for the coactivator in the cytoplasmatic-nuclear-transport of these proteins associated to cytoskeleton. These results demonstrate that there are several molecular pathways that could be affected by their over-expression, including those not restricted to steroid regulation or the nuclear action of coactivators, which results in diminished sensitivity to apoptosis. Furthermore, this could represent one mechanism by which coactivators contribute to tumor development. |
publishDate |
2007 |
dc.date.none.fl_str_mv |
2007-10 |
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/11336/104934 Colo, Georgina Pamela; Rubio, María Fernanda; Nojek Barbieri, Ignacio Martin; Werbajh, Santiago Enrique; Echeverria, Pablo Christian; et al.; The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action; Nature Publishing Group; Oncogene; 27; 17; 10-2007; 2430-2444 0950-9232 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/104934 |
identifier_str_mv |
Colo, Georgina Pamela; Rubio, María Fernanda; Nojek Barbieri, Ignacio Martin; Werbajh, Santiago Enrique; Echeverria, Pablo Christian; et al.; The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action; Nature Publishing Group; Oncogene; 27; 17; 10-2007; 2430-2444 0950-9232 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/1210900 info:eu-repo/semantics/altIdentifier/doi/10.1038/sj.onc.1210900 |
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/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Nature Publishing Group |
publisher.none.fl_str_mv |
Nature Publishing Group |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.13397 |