المستودع الأكاديمي جامعة المدينة

Characterization of dSnoN and its relationship to Decapentaplegic signaling in Drosophila

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dc.contributor Fundación Ramón Areces
dc.contributor Ministerio de Ciencia y Tecnología (España)
dc.contributor Ministerio de Educación y Ciencia (España)
dc.contributor Ministerio de Educación (España)
dc.contributor Gobierno Vasco
dc.creator Barrio, Rosa
dc.creator López-Varea, Ana
dc.creator Casado, Mar
dc.creator Celis, José F. de
dc.date 2008-06-02T14:57:04Z
dc.date 2008-06-02T14:57:04Z
dc.date 2007-03-03
dc.date.accessioned 2017-01-31T01:32:31Z
dc.date.available 2017-01-31T01:32:31Z
dc.identifier Developmental Biology Vol.306, Issue 1, 1 June 2007, Pages 66-81
dc.identifier 0012-1606 (Print)
dc.identifier 1095-564X (Online)
dc.identifier http://hdl.handle.net/10261/4736
dc.identifier 10.1016/j.ydbio.2007.02.039
dc.identifier.uri http://dspace.mediu.edu.my:8181/xmlui/handle/10261/4736
dc.description 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
dc.description J.F.dC. is supported by an institutional grant from the Ramón Areces Foundation for the Centro de Biología Molecular “Severo Ochoa” and by the Ministerio de Ciencia y Tecnología (BMC 2003-01787). R.B. belongs to the Cajal Program (MEC) and is recipient of grants from the Spanish Ministry of Education (BFU2005-00257) and from the Department of Industry, Tourism and Trade of the Government of the Autonomous Community of the Basque Country (Etortek Research Programs 2005/2006) and from the Innovation Technology Department of the Bizkaia County
dc.description Peer reviewed
dc.format 1021029 bytes
dc.format application/pdf
dc.language eng
dc.publisher Elsevier
dc.relation http://dx.doi.org/10.1016/j.ydbio.2007.02.039
dc.rights openAccess
dc.subject TGFβ
dc.subject Decapentaplegic
dc.subject Wing development
dc.subject Ski/SnoN
dc.subject Mad
dc.subject Medea
dc.subject dSmad2
dc.subject Drosophila
dc.title Characterization of dSnoN and its relationship to Decapentaplegic signaling in Drosophila
dc.type Artículo


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