Parkin-mediated selective mitochondrial autophagy, mitophagy: Parkin purges damaged organelles from the vital mitochondrial network.
Cellular homeostasis is linked tightly to mitochondrial functions. Some damage to mitochondrial proteins and nucleic acids can lead to the depolarization of the inner mitochondrial membrane, thereby sensitizing impaired mitochondria for selective elimination by autophagy. Mitochondrial dysfunction is one of the key aspects of the pathobiology of neurodegenerative disease. Parkin, an E3 ligase located in the cytosol and originally discovered as mutated in monogenic forms of Parkinson's disease (PD), was found recently to translocate specifically to uncoupled mitochondria and to induce their autophagy.
Tanaka
Atsushi
A
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-3704, USA. tanakaa@ninds.nih.gov
D000818:Animals; D001343:Autophagy; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D010300:Parkinson Disease / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D021381:Protein Transport; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism*
D044767:Ubiquitin-Protein Ligases; C111567:parkin protein