Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/42991
Campo DC Valoridioma
dc.contributor.authorMenzies, F. M.en_US
dc.contributor.authorGarcia-Arencibia, M.en_US
dc.contributor.authorImarisio, S.en_US
dc.contributor.authorO'Sullivan, N. C.en_US
dc.contributor.authorRicketts, T.en_US
dc.contributor.authorKent, B. A.en_US
dc.contributor.authorRao, M. V.en_US
dc.contributor.authorLam, W.en_US
dc.contributor.authorGreen-Thompson, Z. W.en_US
dc.contributor.authorNixon, R. A.en_US
dc.contributor.authorSaksida, L. M.en_US
dc.contributor.authorBussey, T. J.en_US
dc.contributor.authorO 'Kane, C. J.en_US
dc.contributor.authorRubinsztein, D. C.en_US
dc.contributor.otherGarcia-Arencibia, Moises-
dc.contributor.otherSaksida, Lisa-
dc.contributor.otherBussey, Timothy-
dc.contributor.otherO'Sullivan, Niamh-
dc.contributor.otherKent, Brianne-
dc.date.accessioned2018-11-21T11:59:34Z-
dc.date.available2018-11-21T11:59:34Z-
dc.date.issued2015en_US
dc.identifier.issn1350-9047en_US
dc.identifier.urihttp://hdl.handle.net/10553/42991-
dc.description.abstractOver recent years, accumulated evidence suggests that autophagy induction is protective in animal models of a number of neurodegenerative diseases. Intense research in the field has elucidated different pathways through which autophagy can be upregulated and it is important to establish how modulation of these pathways impacts upon disease progression in vivo and therefore which, if any, may have further therapeutic relevance. In addition, it is important to understand how alterations in these target pathways may affect normal physiology when constitutively modulated over a long time period, as would be required for treatment of neurodegenerative diseases. Here we evaluate the potential protective effect of downregulation of calpains. We demonstrate, in Drosophila, that calpain knockdown protects against the aggregation and toxicity of proteins, like mutant huntingtin, in an autophagy-dependent fashion. Furthermore, we demonstrate that, overexpression of the calpain inhibitor, calpastatin, increases autophagosome levels and is protective in a mouse model of Huntington’s disease, improving motor signs and delaying the onset of tremors. Importantly, long-term inhibition of calpains did not result in any overt deleterious phenotypes in mice. Thus, calpain inhibition, or activation of autophagy pathways downstream of calpains, may be suitable therapeutic targets for diseases like Huntington’s disease.en_US
dc.languageengen_US
dc.publisher1350-9047-
dc.relation.ispartofCell Death and Differentiationen_US
dc.sourceCell Death And Differentiation [ISSN 1350-9047], v. 22 (3), p. 433-444en_US
dc.subject32 Ciencias médicasen_US
dc.subject.otherAutophagyen_US
dc.subject.otherHuntington's diseaseen_US
dc.subject.otherMolecularly targeted therapyen_US
dc.titleCalpain inhibition mediates autophagy-dependent protection against polyglutamine toxicityen_US
dc.typeinfo:eu-repo/semantics/Articlees
dc.typeArticlees
dc.identifier.doi10.1038/cdd.2014.151
dc.identifier.scopus84922506219-
dc.identifier.isi000349543600008-
dcterms.isPartOfCell Death And Differentiation-
dcterms.sourceCell Death And Differentiation[ISSN 1350-9047],v. 22 (3), p. 433-444-
dc.contributor.authorscopusid57203103128-
dc.contributor.authorscopusid15821889300-
dc.contributor.authorscopusid6508213030-
dc.contributor.authorscopusid57205986652
dc.contributor.authorscopusid16245626000-
dc.contributor.authorscopusid50562025300-
dc.contributor.authorscopusid25960969700-
dc.contributor.authorscopusid23969348000-
dc.contributor.authorscopusid56386690700-
dc.contributor.authorscopusid36622132000-
dc.contributor.authorscopusid7102746041-
dc.contributor.authorscopusid6603523140-
dc.contributor.authorscopusid6603730948-
dc.contributor.authorscopusid7004063646-
dc.contributor.authorscopusid7006338728-
dc.contributor.authorscopusid7201740644
dc.description.lastpage444-
dc.description.firstpage433-
dc.relation.volume22-
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000349543600008-
dc.contributor.daisngid395905-
dc.contributor.daisngid4144634-
dc.contributor.daisngid1421159-
dc.contributor.daisngid983219-
dc.contributor.daisngid257867-
dc.contributor.daisngid1106150-
dc.contributor.daisngid1729313-
dc.contributor.daisngid8066453-
dc.contributor.daisngid6604037-
dc.contributor.daisngid29116-
dc.contributor.daisngid245218-
dc.contributor.daisngid187769-
dc.contributor.daisngid322708-
dc.contributor.daisngid37428-
dc.identifier.investigatorRIDK-9920-2013-
dc.identifier.investigatorRIDM-2753-2016-
dc.identifier.investigatorRIDM-2758-2016-
dc.identifier.investigatorRIDNo ID-
dc.identifier.investigatorRIDNo ID-
dc.date.coverdateSeptiembre 2015
dc.identifier.ulpgces
dc.description.sjr4,119
dc.description.jcr8,218
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.orcid0000-0002-1618-4487-
crisitem.author.fullNameGarcía Arencibia, Moisés-
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