PRKN and Parkinson disease: The ubiquitination site specificity and topology of Parkin-dependent target modification in response to mitochondrial depolarization in PD has been examined using peptide affinity capture coupled to MS, revealing extensive conservation of Parkin-dependent ubiquitination sites on cytoplasmic domains in mitochondrial outer membrane proteins [137], consistent with a role for these residues in enabling mitophagy following a mitochondrial permeability transition [138].