Apaf1 mediates apoptosis and mitochondrial damage induced by mutant human SOD1s typical of familial amyotrophic lateral sclerosis (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• Apaf1 mediates apoptosis and mitochondrial damage induced by mutant human SOD1s typical of familial amyotrophic lateral sclerosis (Articolo in rivista) (literal)

Anno

• 2006-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

• 10.1016/j.nbd.2005.06.010 (literal)

Alternative label

• Cozzolino M.; Ferri A.; Ferraro E.; Rotilio G.; Cecconi F.; Carrì M.T. (2006)
  Apaf1 mediates apoptosis and mitochondrial damage induced by mutant human SOD1s typical of familial amyotrophic lateral sclerosis
  in Neurobiology of disease
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Cozzolino M.; Ferri A.; Ferraro E.; Rotilio G.; Cecconi F.; Carrì M.T. (literal)

Pagina inizio

• 69 (literal)

Pagina fine

• 79 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 21 (literal)

Rivista

• Neurobiology of disease (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

• 1 (literal)

Note

• ISI Web of Science (WOS) (literal)
• PubMe (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• IN-Roma (literal)

Titolo

• Apaf1 mediates apoptosis and mitochondrial damage induced by mutant human SOD1s typical of familial amyotrophic lateral sclerosis (literal)

Abstract

• Several studies have indicated that apoptotic pathways are responsible for the loss of motor neurons that constitute the hallmark of amyotrophic lateral sclerosis (ALS). In this study, we demonstrate that apoptosis induced by the expression of several mutant Cu,Zn superoxide dismutases (SOD 1) typical of familial ALS is mediated by Apaf1, a scaffold protein involved in neural development. Using, different cell lines of neuronal origin and modulating the expression of both mutant SOD1s and Apaf1, we show that the removal of Apaf1 prevents cells death. Interestingly, intercepting activation of the caspases cascade is also effective in preventing both the mitochondrial damage and the increase in the production of reactive oxygen species induced by fALS-SOD1, even in the presence of cytochrome c release, This death pathway may be crucial also for the pathogenesis of the sporadic form of the disease, where markers of increased oxidative stress and mitochondria damage have been found. (literal)

Prodotto di

• Modelli animali di deficit neurocomportamentale: meccanismi di adattamento a stress - modelli animali (SV.P16.003.001) (Modulo)
• Institute of neuroscience (IN) (Istituto)

Autore CNR

• ALBERTO FERRI (Unità di personale interno)

Incoming links:

Autore CNR di

• ALBERTO FERRI (Unità di personale interno)

Prodotto

• Institute of neuroscience (IN) (Istituto)
• Modelli animali di deficit neurocomportamentale: meccanismi di adattamento a stress - modelli animali (SV.P16.003.001) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Neurobiology of disease (Rivista)