Proteomic analysis of human PARK2 knockout iPSC-derived neurons

Mitochondrial dysfunction plays a major role in the pathogenesis of sporadic Parkinson’s disease (PD) and familial PD caused by mutations in the PARK2 gene. The protein, parkin, is vital for mitochondrial function, but the lack of key PD phenotypes in PARK2 knockout (KO) rodent models has hindered investigations into parkin’s role in PD pathogenesis. Human isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 KO enable studies of the effect of parkin dysfunction in dopaminergic neuronal cultures.