title: The PARLance of Parkinson disease.
abstract: Mitochondrial biology has recently emerged as a key regulatory event in Parkinson disease (PD). Notably, defects in the clearance of damaged mitochondria, termed mitophagy, have been recently highlighted as a possible mechanistic explanation for neuronal loss. We have recently identified the mitochondrial rhomboid, termed PARL, as a regulator of the cells mitophagic response. Further, we have identified PD-linked mutations at a functional site in the PARL gene. Here we discuss the benefit of combining molecular genetic and cell biology approaches in understanding human disease.
authors.affiliation: Department of Biochemistry, University of Toronto, Toronto, ON, Canada. angus.mcquibban@utoronto.ca
authors.forename: G Angus
authors.initials: GA
authors.lastname: McQuibban
authors.forename: Dennis E
authors.initials: DE
authors.lastname: Bulman
mesh_terms: D001343:Autophagy; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism*; D008954:Models, Biological; D010300:Parkinson Disease / Q000201:enzymology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D011494:Protein Kinases / Q000378:metabolism; D000099202:PTEN-Induced Putative Kinase
chemical_list: D024101:Mitochondrial Proteins; D011494:Protein Kinases; D000099202:PTEN-Induced Putative Kinase