PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy

By N. Matsuda, Shigeto Sato, K. Shiba, K. Okatsu, K. Saisho, C. Gautier, Yu-shin Sou, S. Saiki, S. Kawajiri, Fumiaki Sato and 4 more. Journal of Cell Biology, 2010

1,928 citations recorded by the source corpus.

Defective mitochondrial quality control is shown to be a mechanism for neurodegeneration in some forms of Parkinson's disease.

Subfields: Epidemiology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/36052db6540bece3023b45e1049a13e3ffaa4cae

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Citations in the corpus

Mitochondria: In Sickness and in Health (2012, background): “Loss of membrane potential inhibits the degradation of PINK1 and reroutes it to the surfaceofmitochondria,where it accumulatesand recruitsParkin (Kim et al., 2008; Lin and Kang, 2008; Matsuda et al., 2010; Narendra et al., 2010; Vives-Bauza et al., 2010; Ziviani et al., 2010).”
Autophagy: Renovation of Cells and Tissues (2011, background): “When mitochondria are damaged and depolarized, PINK1 becomes stabilized and recruits Parkin to the damaged mitochondria (Matsuda et al., 2010; Narendra et al., 2008; Narendra et al., 2010a; Vives-Bauza et al., 2010).”
Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL (2010, background): “…damage or uncoupling, Parkin relocalizes to mitochondria and can mediate the autophagic elimination of damaged mitochondria (Narendra et al., 2008), which is dependent on PINK1 kinase activity (Geisler et al., 2010; Matsuda et al., 2010; Narendra et al., 2010; Vives-Bauza et al., 2010).”
The Roles of PINK1, Parkin and Mitochondrial Fidelity in Parkinson's Disease (2015, background): “…and its kinase activity is required for Parkin translocation tomitochondria andmitophagy, linking the function of these autosomal recessive PARK gene products to the same biochemical pathway (Geisler et al., 2010a;Matsuda et al., 2010; Narendra et al., 2010b; Vives-Bauza et al., 2010).”
Deciphering the Molecular Signals of PINK1/Parkin Mitophagy. (2016, background): “Parkin's ability to translocate to damaged mitochondria is tied to its ubiquitin ligase activity since catalytically inactive mutants of Parkin seen in PD predominantly remain in the cytosol after PINK1 accumulation [4,6,11].”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “…import and processing by PARL is inhibited, leading to the integration of PINK1 into the outer mitochondrial membrane, which is a prerequisite to recruit parkin for the induction of mitophagy (Jin et al , 2010; Matsuda et al , 2010; Narendra et al , 2010b; Meissner et al , 2011) (see below).”
p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both (2010, background): “PINK1 accumulates selectively on mitochondria with low membrane potential by inhibition of constitutive voltage-dependent proteolysis to recruit Parkin from the cytosol to dysfunctional mitochondria.(9,10) Following recruitment, Parkin induces the mitophagy of the dysfunctional mitochondria.”
Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “Studies have demonstrated that the expression of PINK1 is necessary for the recruitment of Parkin to depolarized mitochondria.(92,94) However, exactly how accumulation of PINK1 on the outer mitochondrial membrane results in recruitment and activation of Parkin is currently unclear.”
Metabolic regulation of mitochondrial dynamics (2016, background): “Because protein import is dependent on mitochondrial membrane potential, depolarization results in accumulation of Pink1 on the outer membrane (Matsuda et al., 2010; Narendra et al., 2010).”
Cellular mitophagy: Mechanism, roles in diseases and small molecule pharmacological regulation (2023, background): “that PINK1 can significantly accumulate on the surface of the mitochondrial membrane with reduced potential, indicating that it may be the main detector of mitochondrial damage [18].”
Ubiquitination and selective autophagy (2012, background): “Concordantly, translocation of Parkin to uncoupled mitochondria and also its induction seems to be activated by PTEN-induced putative kinase 1.(78,80,81)”