000032770 001__ 32770
000032770 005__ 20170620150449.0
000032770 0247_ $$2doi$$a10.1371/journal.pone.0134830
000032770 0248_ $$2sideral$$a92312
000032770 037__ $$aART-2015-92312
000032770 041__ $$aeng
000032770 100__ $$0(orcid)0000-0003-0156-4230$$aOliván, S.
000032770 245__ $$aTime-point dependent activation of autophagy and the UPS in SOD1G93A mice skeletal muscle
000032770 260__ $$c2015
000032770 5060_ $$aAccess copy available to the general public$$fUnrestricted
000032770 5203_ $$aAmyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by a selective loss of motor neurons together with a progressive muscle weakness. Albeit the pathophysiological mechanisms of the disease remain unknown, growing evidence suggests that skeletal muscle can be a target of ALS toxicity. In particular, the two main intracellular degradation mechanisms, autophagy and the ubiquitin-proteasome degradative system (UPS) have been poorly studied in this tissue. In this study we investigated the activation of autophagy and the UPS as well as apoptosis in the skeletal muscle from SOD1G93A mice along disease progression. Our results showed a significant upregulation of proteasome activity at early symptomatic stage, while the autophagy activation was found at presymptomatic and terminal stages. The mRNA upregulated levels of LC3, p62, Beclin1, Atg5 and E2f1 were only observed at symptomatic and terminal stages, which reinforced the time-point activation of autophagy. Furthermore, no apoptosis activation was observed along disease progression. The combined data provided clear evidence for the first time that there is a time-point dependent activation of autophagy and UPS in the skeletal muscle from SOD1G93A mice.
000032770 536__ $$9info:eu-repo/grantAgreement/ES/FIS/PI14-00947
000032770 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000032770 590__ $$a3.057$$b2015
000032770 591__ $$aMULTIDISCIPLINARY SCIENCES$$b11 / 60 = 0.183$$c2015$$dQ1$$eT1
000032770 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000032770 700__ $$0(orcid)0000-0001-5193-7782$$aCalvo, A.C.$$uUniversidad de Zaragoza
000032770 700__ $$0(orcid)0000-0003-3069-9994$$aGasco, S.
000032770 700__ $$0(orcid)0000-0001-8301-6902$$aMuñoz, M.J.$$uUniversidad de Zaragoza
000032770 700__ $$0(orcid)0000-0001-5740-0185$$aZaragoza, P.$$uUniversidad de Zaragoza
000032770 700__ $$0(orcid)0000-0001-5687-6704$$aOsta, R.$$uUniversidad de Zaragoza
000032770 7102_ $$11005$$2315$$aUniversidad de Zaragoza$$bDepartamento de Farmacología y Fisiología$$cFarmacología
000032770 7102_ $$11001$$2420$$aUniversidad de Zaragoza$$bDepartamento de Anatomía, Embriología y Genética Animal$$cGenética
000032770 773__ $$g10, 8 (2015), 0134830 [15 p.]$$pPLoS One$$tPLoS One$$x1932-6203
000032770 8564_ $$s6438847$$uhttp://zaguan.unizar.es/record/32770/files/texto_completo.pdf$$yVersión publicada
000032770 8564_ $$s96929$$uhttp://zaguan.unizar.es/record/32770/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000032770 909CO $$ooai:zaguan.unizar.es:32770$$particulos$$pdriver
000032770 951__ $$a2017-06-20-14:56:42
000032770 980__ $$aARTICLE