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dc.contributor.authorKnecht, Erwin-
dc.contributor.authorAguado, Carmen-
dc.contributor.authorSarkar, Sovan-
dc.contributor.authorKorolchuk, Viktor I.-
dc.contributor.authorCriado-García, Olga-
dc.contributor.authorVernia, Santiago-
dc.contributor.authorBoya, Patricia-
dc.contributor.authorSanz, Pascual-
dc.contributor.authorRodríguez de Córdoba, Santiago-
dc.contributor.authorRubinsztein, David C.-
dc.date.accessioned2012-07-09T12:47:10Z-
dc.date.available2012-07-09T12:47:10Z-
dc.date.issued2010-10-01-
dc.identifier.citationAutophagy 6(7): 991-993 (2010)es_ES
dc.identifier.issn1554-8627-
dc.identifier.urihttp://hdl.handle.net/10261/53039-
dc.description3 páginas, 1 figura -- PAGS nros. 991-993es_ES
dc.description.abstractLafora disease (LD) is a progressive, lethal, autosomal recessive, neurode- generative disorder that manifests with myoclonus epilepsy. LD is characterized by the presence of intracellular inclusion bodies called Lafora bodies (LB),in brain, spinal cord and other tissues. More than 50 percent of LD is caused by mutations in EPM2A that encodes laforin. Here we review our recent findings that revealed that laforin regulates autophagy. We consider how autophagy compromise may predispose to LB formation and odegeneration in LD, and discuss future investigations suggested by our dataes_ES
dc.description.sponsorshipWork in EK’s lab was supported by grants from the Spanish Ministry of Science and Innovation (BFU2008-00186BMC) and the Instituto de Salud Carlos III (Intramural Project, CIBERER)es_ES
dc.language.isoenges_ES
dc.publisherLandes Biosciencees_ES
dc.rightsclosedAccesses_ES
dc.subjectAutophagyes_ES
dc.subjectglycogen metabolismes_ES
dc.subjectLafora diseasees_ES
dc.subjectlaforines_ES
dc.subjectmalines_ES
dc.subjectneurogenerationes_ES
dc.titleImpaired autophagy in Lafora diseasees_ES
dc.typeartículoes_ES
dc.identifier.doi10.4161/auto.6.7.13308-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.4161/auto.6.7.13308es_ES
dc.identifier.e-issn1554-8635-
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