2016
DOI: 10.1016/j.tcb.2016.05.008
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Deciphering the Molecular Signals of PINK1/Parkin Mitophagy

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Cited by 514 publications
(378 citation statements)
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References 90 publications
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“…PINK1 accumulates on the surface of dysfunctional mitochondria where it simultaneously recruits and activates the E3 ubiquitin ligase activity of Parkin. Parkin ubiquitylates itself and other outer mitochondrial membrane proteins that serve as binding partners of p62, an adaptor molecule that interacts with LC3 to culminate in the engulfment of damaged mitochondria within autophagosomes for degradation 188,189 . PINK1 also has a crucial role in the maintenance of mitochondrial morphology and function, thus models of PINK1 deficiency result in impaired electron transport chain function, altered mitochondrial fusion-fission dynamics, increased oxidative stress and insufficient mitophagy 190 .…”
Section: Targets and Therapeutic Interventions For Mitochondrial Damagementioning
confidence: 99%
“…PINK1 accumulates on the surface of dysfunctional mitochondria where it simultaneously recruits and activates the E3 ubiquitin ligase activity of Parkin. Parkin ubiquitylates itself and other outer mitochondrial membrane proteins that serve as binding partners of p62, an adaptor molecule that interacts with LC3 to culminate in the engulfment of damaged mitochondria within autophagosomes for degradation 188,189 . PINK1 also has a crucial role in the maintenance of mitochondrial morphology and function, thus models of PINK1 deficiency result in impaired electron transport chain function, altered mitochondrial fusion-fission dynamics, increased oxidative stress and insufficient mitophagy 190 .…”
Section: Targets and Therapeutic Interventions For Mitochondrial Damagementioning
confidence: 99%
“…Under healthy conditions, Parkin has been proposed to protect dopaminergic neurons by promoting mitochondrial homeostasis in a PGC-1α-dependent manner (Zheng et al, 2017). Furthermore, Mfn2 has been reported to function as a receptor for Parkin in cardiac cells (Chen & Dorn, 2013;Gong et al, 2015), however whether this extends beyond this cell type is unclear (Narendra et al, 2008;Nguyen et al, 2016). Overall, these data provide a significant link between Mfn2 regulation and PD.…”
Section: (2) Additional Neurodegenerative Diseasesmentioning
confidence: 88%
“…Mutations in two mitochondrial genes, PINK1 and Parkin, are causal for hereditary PD, linking mitochondrial dysfunction to this disease (Kitada et al, 1998;Valente et al, 2004;Dodson & Guo, 2007). Mfn2 is a key ubiquitination target of Parkin (Matsuda et al, 2010;Nguyen, Padman & Lazarou, 2016), and Parkin mediates the expression of PGC-1α (Shin et al, 2011), which in turn controls Mfn2 expression under stress conditions (see Section IV) (Bach et al, 2003Soriano et al, 2006). Under healthy conditions, Parkin has been proposed to protect dopaminergic neurons by promoting mitochondrial homeostasis in a PGC-1α-dependent manner (Zheng et al, 2017).…”
Section: (2) Additional Neurodegenerative Diseasesmentioning
confidence: 99%
“…Many of these diverse receptors are known to interact with LC3B, the classical marker of the autophagic membrane, via LC3-interacting region (LIR) motifs, as mentioned above [55]. For example, the identification of clearly defined roles for the mitochondrial cargo receptors NDP52 and optineurin have provided exciting new insights into the selective process of mitophagy [56,57]. In addition to NDP52 [58], which may play roles in other types of autophagy such as xenophagy [59], general candidate receptors for the targeted turnover of other cellular organelles have also been identified, including p62/SQSTM1, NBR1, and Huntingtin [6062].…”
Section: Proteins Involved In Lipophagy Inductionmentioning
confidence: 99%