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  2. FCEN
  3. FCEN - Facultad de Ciencias Exactas y Naturales. UBA
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dc.provenanceFacultad de Ciencias Exactas y Naturales de la UBA-
dc.contributor<div class="autor_fcen" id="5349">Marazita, M.C.</div>-
dc.contributor<div class="autor_fcen" id="6215">Florencia Ogara, M.</div>-
dc.contributor<div class="autor_fcen" id="8224">Sonzogni, S.V.</div>-
dc.contributor<div class="autor_fcen" id="5439">Martí, M.</div>-
dc.contributor<div class="autor_fcen" id="2719">Dusetti, N.J.</div>-
dc.contributor<div class="autor_fcen" id="6746">Pignataro, O.P.</div>-
dc.contributor<div class="autor_fcen" id="1416">Cánepa, E.T.</div>-
dc.creator<div class="autor_fcen" id="5349">Marazita, M.C.</div>-
dc.creator<div class="autor_fcen" id="6215">Florencia Ogara, M.</div>-
dc.creator<div class="autor_fcen" id="8224">Sonzogni, S.V.</div>-
dc.creator<div class="autor_fcen" id="5439">Martí, M.</div>-
dc.creator<div class="autor_fcen" id="2719">Dusetti, N.J.</div>-
dc.creator<div class="autor_fcen" id="6746">Pignataro, O.P.</div>-
dc.creator<div class="autor_fcen" id="1416">Cánepa, E.T.</div>-
dc.date.accessioned2018-05-04T21:59:58Z-
dc.date.accessioned2018-05-28T15:49:17Z-
dc.date.available2018-05-04T21:59:58Z-
dc.date.available2018-05-28T15:49:17Z-
dc.date.issued2012-
dc.identifier.urihttp://10.0.0.11:8080/jspui/handle/bnmm/68627-
dc.descriptionDNA damage triggers a phosphorylation-based signaling cascade known as the DNA damage response. p19INK4d, a member of the INK4 family of CDK4/6 inhibitors, has been reported to participate in the DNA damage response promoting DNA repair and cell survival. Here, we provide mechanistic insight into the activation mechanism of p19INK4d linked to the response to DNA damage. Results showed that p19INK4d becomes phosphorylated following UV radiation, b-amyloid peptide and cisplatin treatments. ATM-Chk2/ATR-Chk1 signaling pathways were found to be differentially involved in p19INK4d phosphorylation depending on the type of DNA damage. Two sequential phosphorylation events at serine 76 and threonine 141 were identified using p19INK4d single-point mutants in metabolic labeling assays with 32P-orthophosphate. CDK2 and PKA were found to participate in p19INK4d phosphorylation process and that they would mediate serine 76 and threonine 141 modifications respectively. Nuclear translocation of p19INK4d induced by DNA damage was shown to be dependent on serine 76 phosphorylation. Most importantly, both phosphorylation sites were found to be crucial for p19INK4d function in DNA repair and cell survival. In contrast, serine 76 and threonine 141 were dispensable for CDK4/6 inhibition highlighting the independence of p19INK4d functions, in agreement with our previous findings. These results constitute the first description of the activation mechanism of p19INK4d in response to genotoxic stress and demonstrate the functional relevance of this activation following DNA damage. © 2012 Marazita et al.-
dc.descriptionFil:Marazita, M.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Florencia Ogara, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Sonzogni, S.V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Martí, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Dusetti, N.J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Pignataro, O.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Cánepa, E.T. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.formatapplication/pdf-
dc.languageeng-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttp://creativecommons.org/licenses/by/2.5/ar-
dc.sourcePLoS ONE 2012;7(4)-
dc.source.urihttp://digital.bl.fcen.uba.ar/Download/paper/paper_19326203_v7_n4_p_Marazita.pdf-
dc.subjectamyloid beta protein-
dc.subjectATM protein-
dc.subjectATR protein-
dc.subjectcheckpoint kinase 1-
dc.subjectcheckpoint kinase 2-
dc.subjectcisplatin-
dc.subjectcyclic AMP dependent protein kinase-
dc.subjectcyclin dependent kinase 2-
dc.subjectcyclin dependent kinase 4-
dc.subjectcyclin dependent kinase 6-
dc.subjectcyclin dependent kinase inhibitor 2D-
dc.subjectphosphate p 32-
dc.subjectserine-
dc.subjectthreonine-
dc.subjectamyloid beta protein-
dc.subjectCDK2 protein, human-
dc.subjectcisplatin-
dc.subjectcyclic AMP dependent protein kinase-
dc.subjectcyclin dependent kinase 2-
dc.subjectcyclin dependent kinase inhibitor 2D-
dc.subjectDNA-
dc.subjectarticle-
dc.subjectcell nucleus-
dc.subjectcell survival-
dc.subjectconformational transition-
dc.subjectcontrolled study-
dc.subjectDNA damage-
dc.subjectDNA repair-
dc.subjectpoint mutation-
dc.subjectprotein phosphorylation-
dc.subjectsignal transduction-
dc.subjectultraviolet radiation-
dc.subjectcell cycle-
dc.subjectcell line-
dc.subjectcell strain HEK293-
dc.subjectDNA damage-
dc.subjectDNA repair-
dc.subjectdrug effect-
dc.subjectgene expression regulation-
dc.subjectgenetics-
dc.subjecthuman-
dc.subjectmetabolism-
dc.subjectmutation-
dc.subjectphosphorylation-
dc.subjectprotein transport-
dc.subjectradiation exposure-
dc.subjectAmyloid beta-Peptides-
dc.subjectCell Cycle-
dc.subjectCell Line-
dc.subjectCell Survival-
dc.subjectCisplatin-
dc.subjectCyclic AMP-Dependent Protein Kinases-
dc.subjectCyclin-Dependent Kinase 2-
dc.subjectCyclin-Dependent Kinase Inhibitor p19-
dc.subjectDNA-
dc.subjectDNA Damage-
dc.subjectDNA Repair-
dc.subjectGene Expression Regulation-
dc.subjectHEK293 Cells-
dc.subjectHumans-
dc.subjectMutation-
dc.subjectPhosphorylation-
dc.subjectProtein Transport-
dc.subjectSignal Transduction-
dc.subjectUltraviolet Rays-
dc.titleCDK2 and PKA mediated-sequential phosphorylation is critical for p19INK4d function in the DNA damage response-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:ar-repo/semantics/artículo-
dc.typeinfo:eu-repo/semantics/publishedVersion-
Aparece en las colecciones: FCEN - Facultad de Ciencias Exactas y Naturales. UBA

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