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Inefficient DNA repair is an aging-related modifier of parkinson's disease

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dc.creatorSepe, Sara
dc.creatorMilanese, Chiara
dc.creatorGabriels, Sylvia
dc.creatorDerks, Kasper W.J.
dc.creatorPayan-Gomez, Cesar
dc.creatorvan IJcken, Wilfred F.J.
dc.creatorRijksen, Yvonne M.A.
dc.creatorNigg, Alex L.
dc.creatorMoreno, Sandra
dc.creatorCerri, Silvia
dc.creatorBlandini, Fabio
dc.creatorHoeijmakers, Jan H.J.
dc.creatorMastroberardino, Pier G.
dc.creator.googleSepe, Saraspa
dc.creator.googleMilanese, Chiaraspa
dc.creator.googleGabriels, Sylviaspa
dc.creator.googleDerks, Kasper W.J.spa
dc.creator.googlePayan-Gomez, Cesarspa
dc.creator.googlevan IJcken, Wilfred F.J.spa
dc.creator.googleRijksen, Yvonne M.A.spa
dc.creator.googleNigg, Alex L.spa
dc.creator.googleMoreno, Sandraspa
dc.creator.googleCerri, Silviaspa
dc.creator.googleBlandini, Fabiospa
dc.creator.googleHoeijmakers, Jan H.J.spa
dc.creator.googleMastroberardino, Pier G.spa
dc.date.accessioned2019-01-28T16:50:47Z
dc.date.available2019-01-28T16:50:47Z
dc.date.created2016
dc.date.issued2016
dc.description.abstractThe underlying relation between Parkinson's disease (PD) etiopathology and its major risk factor, aging, is largely unknown. In light of the causative link between genome stability and aging, we investigate a possible nexus between DNA damage accumulation, aging, and PD by assessing aging-related DNA repair pathways in laboratory animal models and humans. We demonstrate that dermal fibroblasts from PD patients display flawed nucleotide excision repair (NER) capacity and that Ercc1 mutant mice with mildly compromised NER exhibit typical PD-like pathological alterations, including decreased striatal dopaminergic innervation, increased phospho-synuclein levels, and defects in mitochondrial respiration. Ercc1 mouse mutants are also more sensitive to the prototypical PD toxin MPTP, and their transcriptomic landscape shares important similarities with that of PD patients. Our results demonstrate that specific defects in DNA repair impact the dopaminergic system and are associated with human PD pathology and might therefore constitute an age-related risk factor for PD. © 2016 The Author(s).eng
dc.format.mimetypeapplication/pdf
dc.identifier.issnISSN 2211-1247
dc.identifier.urihttp://repository.urosario.edu.co/handle/10336/18940
dc.language.isoengspa
dc.relation.citationEndPage1875
dc.relation.citationIssueNo. 9
dc.relation.citationStartPage1866
dc.relation.citationTitleCell Reports
dc.relation.citationVolumeVol. 15
dc.relation.ispartofCell Reports, ISSN: 2211-1247, Vol. 15/No. 9 (2016) pp. 1866-1875spa
dc.relation.urihttps://ac.els-cdn.com/S2211124716305150/1-s2.0-S2211124716305150-main.pdf?_tid=74816f58-bdc3-4f49-a06f-2cbc9410de11&acdnat=1540055928_56ba66e2a443310cccef7b985f953dfbspa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.rights.cchttps://creativecommons.org/licenses/by-nc-nd/4.0/spa
dc.source.bibliographicCitationAhmad, A., Robinson, A.R., Duensing, A., van Drunen, E., Beverloo, H.B., Weisberg, D.B., Hasty, P., Niedernhofer, L.J., ERCC1-XPF endonuclease facilitates DNA double-strand break repair (2008) Mol. Cell. Biol., 28, pp. 5082-5092spa
dc.source.instnameinstname:Universidad del Rosario
dc.source.reponamereponame:Repositorio Institucional EdocUR
dc.subjectAlpha Synucleinspa
dc.subjectCre Recombinasespa
dc.subjectExcision Repair Cross Complementing Protein 1spa
dc.subjectHistone H2Axspa
dc.subjectHistone H2Ax Gammaspa
dc.subjectUnclassified Drugspa
dc.subjectDna Binding Proteinspa
dc.subjectEndonucleasespa
dc.subjectAgingspa
dc.subjectAnimal Experimentspa
dc.subjectAnimal Modelspa
dc.subjectAutonomic Innervationspa
dc.subjectControlled Studyspa
dc.subjectDisease Associationspa
dc.subjectDna Damagespa
dc.subjectDna Repairspa
dc.subjectDopaminergic Systemspa
dc.subjectDouble Stranded Dna Breakspa
dc.subjectDown Regulationspa
dc.subjectEnzyme Activityspa
dc.subjectErcc1 Genespa
dc.subjectExcision Repairspa
dc.subjectGene Expressionspa
dc.subjectGene Mutationspa
dc.subjectHumanspa
dc.subjectHuman Cellspa
dc.subjectMitochondrial Respirationspa
dc.subjectMousespa
dc.subjectNeuropathologyspa
dc.subjectNonhumanspa
dc.subjectOxidation Reduction Statespa
dc.subjectParkinson Diseasespa
dc.subjectPriority Journalspa
dc.subjectProtein Expressionspa
dc.subjectProtein Homeostasisspa
dc.subjectProtein Phosphorylationspa
dc.subjectRna Sequencespa
dc.subjectSkin Fibroblastspa
dc.subjectUpregulationspa
dc.subjectAgingspa
dc.subjectAnimalspa
dc.subjectCorpus Striatumspa
dc.subjectDopaminergic Nerve Cellspa
dc.subjectFibroblastspa
dc.subjectMetabolismspa
dc.subjectParkinson Diseasespa
dc.subjectPathologyspa
dc.subjectUltrastructurespa
dc.subjectAgingspa
dc.subjectAnimalsspa
dc.subjectCorpus Striatumspa
dc.subjectDna Repairspa
dc.subjectDna-Binding Proteinsspa
dc.subjectDopaminergic Neuronsspa
dc.subjectEndonucleasesspa
dc.subjectFibroblastsspa
dc.subjectMicespa
dc.subjectParkinson Diseasespa
dc.subject.ddcEnfermedadesspa
dc.subject.keywordMouseeng
dc.subject.keywordErcc1 Proteineng
dc.subject.keywordArticlespa
dc.subject.keywordHumansspa
dc.subject.lembEnfermedad de parkinsonspa
dc.subject.lembEdad adultaspa
dc.subject.lembVejezspa
dc.titleInefficient DNA repair is an aging-related modifier of parkinson's diseasespa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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