title: Pathologic and therapeutic implications for the cell biology of parkin.
abstract: Mutations in the E3 ligase parkin are the most common cause of autosomal recessive Parkinson's disease (PD), but it is believed that parkin dysfunction may also contribute to idiopathic PD. Since its discovery, parkin has been implicated in supporting multiple neuroprotective pathways, many revolving around the maintenance of mitochondrial health quality control and governance of cell survival. Recent advances across the structure, biochemistry, and cell biology of parkin have provided great insights into the etiology of parkin-linked and idiopathic PD and may ultimately generate novel therapeutic strategies to slow or halt disease progression. This review describes the various pathways in which parkin acts and the mechanisms by which parkin may be targeted for therapeutic intervention. This article is part of a Special Issue entitled 'Neuronal Protein'.
authors.affiliation: Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, USA; Harvard Medical School, Boston, USA.
authors.forename: Rakshita A
authors.initials: RA
authors.lastname: Charan
authors.affiliation: Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, USA; Harvard Medical School, Boston, USA.
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: LaVoie
mesh_terms: D000818:Animals; D006801:Humans; D058990:Molecular Targeted Therapy / Q000379:methods*; D009154:Mutation / Q000235:genetics; D010300:Parkinson Disease / Q000235:genetics / Q000473:pathology / Q000628:therapy; D044767:Ubiquitin-Protein Ligases / Q000235:genetics / Q000378:metabolism*
chemical_list: D044767:Ubiquitin-Protein Ligases; C111567:parkin protein
keywords: Apoptosis; Mitophagy; Neurodegeneration; PD; Parkin; Therapy