Calcineurin Controls Cellular Prion Protein Expression in Mouse Astrocytes.

ABSTRACT: Prion diseases arise from the conformational conversion of the cellular prion protein (PrP^C) into a self-replicating prion isoform (PrP^Sc). Although this process has been studied mostly in neurons, a growing body of evidence suggests that astrocytes express PrP^C and are able to replicate and accumulate PrP^Sc. Currently, prion diseases remain incurable, while downregulation of PrP^C represents the most promising therapy due to the reduction of the substrate for prion conversion. Here we show that the astrocyte-specific genetic ablation or pharmacological inhibition of the calcium-activated phosphatase calcineurin (CaN) reduces PrP^C expression in astrocytes. Immunocytochemical analysis of cultured CaN-KO astrocytes and isolatio

SUBMITTER: Dematteis G 

PROVIDER: S-EPMC8870693 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature