Brain injury-induced proteolysis is reduced in a novel calpastatin-overexpressing transgenic mouse.

ABSTRACT: The calpain family of calcium-dependent proteases has been implicated in a variety of diseases and neurodegenerative pathologies. Prolonged activation of calpains results in proteolysis of numerous cellular substrates including cytoskeletal components and membrane receptors, contributing to cell demise despite coincident expression of calpastatin, the specific inhibitor of calpains. Pharmacological and gene-knockout strategies have targeted calpains to determine their contribution to neurodegenerative pathology; however, limitations associated with treatment paradigms, drug specificity, and genetic disruptions have produced inconsistent results and complicated interpretation. Specific, targeted calpain inhibition achieved by enhancing endogenous calpastatin levels offers unique advantages

SUBMITTER: Schoch KM 

PROVIDER: S-EPMC3676438 | biostudies-literature | 2013 Jun

REPOSITORIES: biostudies-literature