English   español  
Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/4736
Compartir / Impacto:
Estadísticas
Add this article to your Mendeley library MendeleyBASE
Citado 7 veces en Web of Knowledge®  |  Pub MebCentral Ver citas en PubMed Central  |  Ver citas en Google académico
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar otros formatos: Exportar EndNote (RIS)Exportar EndNote (RIS)Exportar EndNote (RIS)
Título : Characterization of dSnoN and its relationship to Decapentaplegic signaling in Drosophila
Autor : Barrio, Rosa; López-Varea, Ana; Casado, Mar; Celis, José F. de
Palabras clave : TGFβ
Decapentaplegic
Wing development
Ski/SnoN
Mad
Medea
dSmad2
Drosophila
Fecha de publicación : 3-mar-2007
Editor: Elsevier
Citación : Developmental Biology Vol.306, Issue 1, 1 June 2007, Pages 66-81
Resumen: Vertebrate members of the ski/snoN family of proto-oncogenes antagonize TGFβ and BMP signaling in a variety of experimental situations. This activity of Ski/SnoN proteins is related to their ability to interact with Smads, the proteins acting as key mediators of the transcriptional response to the TGFβ superfamily members. However, despite extensive efforts to identify the physiological roles of the Ski/SnoN proteins, it is not yet clear whether they participate in regulating Activin and/or BMP signaling during normal development. It is therefore crucial to examine their roles in vivo mostly because of the large number of known Ski/SnoN-interacting proteins and the association between the up-regulation of these genes and cancer progression. Here we characterize the Drosophila homolog to vertebrate ski and snoN genes. The Drosophila dSnoN protein retains the ability of its vertebrate counterparts to antagonize BMP signaling in vivo and in cultured cells. dSnoN does not interfere with Mad phosphorylation but it interacts genetically with Mad, Medea and dSmad2. Mutations in either the Smad2–3 or Smad4 putative binding sites of dSnoN prevent the antagonism of dSnoN towards Dpp signaling, although homozygous flies for these mutations or for a genetic deficiency of the locus are viable and have wings of normal size and pattern
Versión del editor: http://dx.doi.org/10.1016/j.ydbio.2007.02.039
URI : http://hdl.handle.net/10261/4736
DOI: 10.1016/j.ydbio.2007.02.039
ISSN: 0012-1606 (Print)
1095-564X (Online)
Aparece en las colecciones: (CBM) Artículos
Ficheros en este ítem:
Fichero Descripción Tamaño Formato  
Barrio et al 07.pdf997,1 kBAdobe PDFVista previa
Visualizar/Abrir
Mostrar el registro completo
 



NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.