SOD1 Lysine 123 Acetylation in the Adult Central Nervous System.

ABSTRACT: Superoxide dismutase 1 (SOD1) knockout (Sod1^-/-) mice exhibit an accelerated aging phenotype. In humans, SOD1 mutations are linked to familial amyotrophic lateral sclerosis (ALS), and post-translational modification (PTM) of wild-type SOD1 has been associated with sporadic ALS. Reversible acetylation regulates many enzymes and proteomic studies have identified SOD1 acetylation at lysine 123 (K123). The function and distribution of K123-acetylated SOD1 (Ac-K123 SOD1) in the nervous system is unknown. Here, we generated polyclonal rabbit antibodies against Ac-K123 SOD1. Sod1 deletion in Sod1^-/- mice, K123 mutation or preabsorption with Ac-K123 peptide all abolished antibody binding. Using immunohistochemistry, we assessed Ac-K123 SOD1 distrib

SUBMITTER: Kaliszewski M 

PROVIDER: S-EPMC5167747 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature