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dc.contributor.author
Dennler, Sylviane
dc.contributor.author
Pendaries, Valérie
dc.contributor.author
Tacheau, Charlotte
dc.contributor.author
Costas, Monica Alejandra
dc.contributor.author
Mauviel, Alain
dc.contributor.author
Verrecchia, Franck
dc.date.available
2020-06-29T20:36:37Z
dc.date.issued
2005-01
dc.identifier.citation
Dennler, Sylviane; Pendaries, Valérie; Tacheau, Charlotte; Costas, Monica Alejandra; Mauviel, Alain; et al.; The steroid receptor co-activator-1 (SRC-1) potentiates TGF-β/Smad signaling: role of p300/CBP; Nature Publishing Group; Oncogene; 24; 11; 1-2005; 1936-1945
dc.identifier.issn
0950-9232
dc.identifier.uri
http://hdl.handle.net/11336/108439
dc.description.abstract
The three related 160-kDa proteins, SRC-1, TIF-2 and RAC-3, were initially identi•ed as factors interacting with nuclear receptors. They have also been reported to potentiate the activity of other transcription factors such as AP-1 or NF-jB. The aimof this work was to identify whether SRC-1 interferes with the TGF-b/Smad signaling pathway, and if so, to identify its underlying mechanisms of action. Using transient cell transfection experiments performed in human dermal •broblasts with the Smad3/4- speci•c (SBE)4-lux reporter construct, as well as the human PAI-1 promoter, we determined that SRC-1 enhances TGF-b-induced, Smad-mediated, transcription. Likewise, SRC-1 overexpression potentiated TGF-binduced upregulation of PAI-1 steady-state mRNA levels. Using a mammalian two-hybrid system, we demonstrated that SRC-1 interacts with the transcriptional co-activators p300/CBP, but not with Smad3. Overexpression of the adenovirus E1A oncoprotein, an inhibitor of CBP/ p300 activity, prevented the enhancing effect of SRC-1 on Smad3/4-mediated transcription, indicating that p300/ CBP may be required for SRC-1 effect. Such hypothesis was validated, as expression of a mutant form of SRC-1 lacking the CBP/p300-binding site failed to upregulate Smad3/4-dependent transcription, while full-length SRC- 1 potentiated p300 . Smad3 interactions. These results identify SRC-1 as a novel Smad3/4 transcriptional partner, facilitating the functional link between Smad3 and p300/CBP.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Nature Publishing Group
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
p300
dc.subject
Smad
dc.subject
SRC-1 TGF-b
dc.subject.classification
Otras Ciencias Médicas
dc.subject.classification
Otras Ciencias Médicas
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
The steroid receptor co-activator-1 (SRC-1) potentiates TGF-β/Smad signaling: role of p300/CBP
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-06-23T14:53:07Z
dc.journal.volume
24
dc.journal.number
11
dc.journal.pagination
1936-1945
dc.journal.pais
Reino Unido
dc.journal.ciudad
Londres
dc.conicet.avisoEditorial
Acceso abierto en el enlace propuesto.
dc.description.fil
Fil: Dennler, Sylviane. Hôpital Saint-Louis; Francia. Inserm; Francia
dc.description.fil
Fil: Pendaries, Valérie. Hôpital Saint-Louis; Francia. Inserm; Francia
dc.description.fil
Fil: Tacheau, Charlotte. Inserm; Francia. Hôpital Saint-Louis; Francia
dc.description.fil
Fil: Costas, Monica Alejandra. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Ciencias Biológicas; Argentina. 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
dc.description.fil
Fil: Mauviel, Alain. Hôpital Saint-Louis; Francia. Inserm; Francia
dc.description.fil
Fil: Verrecchia, Franck. Hôpital Saint-Louis; Francia. Inserm; Francia
dc.journal.title
Oncogene
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/1208343
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1038/sj.onc.1208343
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