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Article

Mitochondrial redox signalling by p66Shc mediates ALS-like disease through Rac1 inactivation.

Human molecular genetics - 1 Nov 2011

Pesaresi Maria Grazia, Amori Ilaria, Giorgi Carlotta, Ferri Alberto, Fiorenzo Paolo, Gabanella Francesca, Salvatore Anna Maria, Giorgio Marco, Pelicci Pier Giuseppe, Pinton Paolo, Carrì Maria Teresa, Cozzolino Mauro

Abstract excerpt

Increased oxidative stress and mitochondrial damage are among the mechanisms whereby mutant SOD1 (mutSOD1) associated with familial forms of amyotrophic lateral sclerosis (ALS) induces motoneuronal death. The 66 kDa isoform of the growth factor adapter Shc (p66Shc) is known to be central in the control of mitochondria-dependent oxidative balance. Here we report that expression of mutSOD1s induces the activation...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 21828072
DOI: 10.1093/hmg/ddr347

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SOD1

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Related research

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Mitochondrial redox signalling by p66Shc mediates ALS-like disease through Rac1 inactivation.PMID 21828072Read ↗

SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model.Semantic proximity Read ↗

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The molecular pathogenesis of superoxide dismutase 1-linked ALS is promoted by low oxygen tensionSemantic proximity Read ↗

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