Loss-of-function mutations in parkin are the predominant cause of familial Parkinson's
disease. We previously reported that parkin-/-mice exhibit nigrostriatal deficits in the
absence of nigral degeneration. Parkin has been shown to function as an E3 ubiquitin
ligase. Loss of parkin function, therefore, has been hypothesized to cause nigral
degeneration via an aberrant accumulation of its substrates. Here we employed a proteomic
approach to determine whether loss of parkin function results in alterations in abundance …