Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10801849 | Biochimica et Biophysica Acta (BBA) - Molecular Cell Research | 2015 | 5 Pages |
Abstract
Autophagy is an intracellular catabolic system that degrades cytoplasmic proteins and organelles. Damaged mitochondria can be degraded by a selective type of autophagy, which is termed mitophagy. PINK1-Parkin-dependent mitophagy has been extensively studied in the mammalian system. PINK1 accumulates on damaged mitochondria to recruit Parkin, which subsequently ubiquitinates a broad range of outer mitochondrial membrane proteins. Ubiquitinated mitochondria associate with the autophagosome formation site, and are selectively incorporated into autophagosomes. During this process, damaged mitochondria first associate with the autophagosome formation site together with upstream autophagy factors, then are efficiently incorporated into autophagosomes through binding with autophagosome adaptors. This “two-step model” may be applied to other selective types of autophagy. This article is part of a Special Issue entitled: Mitophagy.
Keywords
NDP52ULK1HDAC6PI3KFIP200SQSTM1sequestosome 1Cdc37FUNDC1PI3POMMSTXSmurf1NCOA4NIXNeighbor of BRCA1 gene 1WIPIDfcp1Tax1BP1VMP1nuclear receptor coactivator 4NBRATGLC3CCCPBNIP3SNAREPINK1Fis1HSP90mTORSelective autophagyPTEN-induced putative kinase 1LIRmicrotubule-associated protein light chain 3syntaxinendoplasmic reticulumGAPouter mitochondrial membranephosphatidylethanolaminePhosphatidylinositol 3-kinasephosphatidylinositol 3-phosphateTwo-step modelautophagy-relatedLC3-interacting regionMitophagyMechanistic target of rapamycinHopsHistone deacetylase 6Parkinmitochondrial fission 1 proteinHeat shock protein 90GTPase-activating proteincarbonyl cyanide m-chlorophenylhydrazoneGABARAPsoluble NSF attachment protein receptor
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Authors
Saori R. Yoshii, Noboru Mizushima,