PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1

By Sven Geisler, Kira M. Holmström, Diana Skujat, F. Fiesel, Oliver C. Rothfuss, P. Kahle, W. Springer. Nature Cell Biology, 2010

2,787 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/5b1235ae110f1903e2c14a71837325c2dd7effd4

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In Epidemiology

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2. D. Klionsky
3. N. Mizushima
4. Guido Kroemer
5. I. Slaninová
6. Alec C. Kimmelman
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In Molecular Biology

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2. Guido Kroemer
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7. D. C. Chan
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In Neurology

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3. Edward A. Fon
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5. D. Klionsky
6. Gian-Luca McLelland
7. W. Ding
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Citations in the corpus

• PINK1 is activated by mitochondrial membrane potential depolarization and stimulates Parkin E3 ligase activity by phosphorylating Serine 65 (2012, background): “It is possible that the key Parkin targets are located at the mitochondria and indeed several candidate mitochondrial substrates for Parkin have been proposed, including Mitofusin1 [35], VDAC1 [12] and more recently PARIS [36] and Miro [37].”
• PINK1 is degraded through the N-end rule pathway (2013, background): “Furthermore, PINK1(1-155)-YFP, a mutant with an N-end stabilizing residue was stably localized in the cytosol (Fig.”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “…adaptor protein p62 (also termed as SQSTM1, sequestosome-1), which links ubiquitinated cargo to the autophagic machinery by binding to both ubiquitin and LC3, has been described as an essential factor for parkin-induced mitophagy (Ding et al , 2010; Geisler et al , 2010a; Lee et al , 2010b).”
• Measuring in vivo mitophagy (2015, background): “…potential has been shown to result in the stabilization of the phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1), which in turn recruits the E3 ubiquitin ligase Parkin to mitochondria and can trigger mitophagy (Geisler et al., 2010; Matsuda et al., 2010; Narendra et al., 2008).”
• The ubiquitin code. (2012, neutral): “, Lys63-linked diubiquitin has been caught in”
• Synaptic energy use and supply. (2012, positive): “When this pathway is deranged, as occurs with mutations in PINK1 or Parkin that give rise to hereditary forms of Parkinson’s disease (Kitada et al., 1998; Valente et al., 2004), malfunctioning mitochondria will not provide sufficient ATP at synapses.”
• Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis. (2011, background): “…tumors. p62 is required for efficient tumorigenesis by Ras The autophagy cargo receptor p62 binds LC3 and Ub on modified proteins, including those on organelles such as depolarized mitochondria, thereby targeting cargo to autophagosomes for degradation (Pankiv et al. 2007; Geisler et al. 2010).”
• Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “Here, PINK1 recruits Parkin(68) that ubiquitylates a number of outer mitochondrial membrane-located proteins, for example, the voltagedependent anion channel 1 (VDAC1).(69) Once ubiquitylated, these proteins are recognized by p62/sequestosome 1 (p62/ SQSTM1, or simply p62),(69,70) a ubiquitin-bindin”
• Mitochondrial dynamics and mitochondrial quality control (2014, background): “In addition to regulating mitochondria fusion and fission, Parkin-induced ubiquitination of Miro induces mitochondrial arrest, which can segregate damaged mitochondria from healthy mitochondria prior to mitophagy [60].”
• The Beclin 1 network regulates autophagy and apoptosis (2011, positive): “It has been implicated in protecting cells from stress-induced mitochondrial dysfunction by regulation of mitophagy.(63) Moreover, the full-length PINK1, but not its cleaved isoforms, or a mutant protein truncated at the C-terminus, interacts with the pro-autophagic protein Beclin 1 and enhances aut”
• PINK1- and Parkin-mediated mitophagy at a glance (2012, background): “…Parkin ubiquitylates numerous outer mitochondrial membrane (OMM) proteins, which in turn recruit other proteins to mitochondria to initiate mitophagy (Chan et al., 2011; Geisler et al., 2010a; Lee et al., 2010b; Narendra et al., 2010a; Tanaka et al., 2010; Yoshii et al., 2011) (see Poster).”