PINK1-dependent recruitment of Parkin to mitochondria in mitophagy

By C. Vives-Bauzá, Chun Zhou, Yong Huang, M. Cui, R. L. de Vries, Jiho Kim, Jessica May, M. Tocilescu, Wencheng Liu, H. Ko and 8 more. Proceedings of the National Academy of Sciences of the United States of America, 2009

1,653 citations recorded by the source corpus.

Subfields: Epidemiology, Neurology

View Paper: https://www.semanticscholar.org/paper/029246bcb9838971376a9cbe05334af4e1659298

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Citations in the corpus

Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy. (2010, methodology): “Since parkin has been shown to be involved in the removal of damaged mitochondria (33,34), the induction of macroautophagy was investigated in PINK1-silenced cells.”
Broad activation of the ubiquitin–proteasome system by Parkin is critical for mitophagy (2011, result): “The bulk of the mitochondria aggregated around the perinuclear region, consistent with previous studies (6,10,17).”
Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “66,67 This subsequently triggers the ubiquitination of mitochondrial proteins, effectively marking these damaged components for removal.”
PINK1 is activated by mitochondrial membrane potential depolarization and stimulates Parkin E3 ligase activity by phosphorylating Serine 65 (2012, background): “In response to mitochondrial membrane potential (Dcm) depolarization, for example induced by the uncoupling agent carbonyl cyanide m-chlorophenyl hydrazone (CCCP), a marked stabilization of full length PINK1 at the mitochondria is observed [12–15].”
Mitochondria ROS and mitophagy in acute kidney injury (2022, background): “PINK1 will phosphorylate PRKN on the Ub-like domain on the Ser resulting in an increase of its E3 activity (Ub ligase activity) and the formation of polyubiquitin chains on the surface of depolarized mitochondrial membranes [49,50].”
Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “PINK1 (PTEN-induced kinase 1) mediates recruitment of parkin to the damaged mitochondria and activates parkin’s ligase activity [144], thereby promoting autophagy.”
Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control (2014, background): “…paradigm, PINK1, a serine/threonine kinase, globally accumulates on depolarized mitochondria and recruits parkin from the cytosol to mitochondria in a manner dependent upon PINK1 phosphorylation activity (Narendra et al, 2008, 2010; Matsuda et al, 2010; Vives-Bauza et al, 2010; Greene et al, 2012).”
PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy (2010, result): “While our manuscript was under review, Geisler et al. (2010), Narendra et al. (2010), and Vives-Bauza et al. (2010) independently published results that are consistent with those described herein.”
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).”
Mechanism of Oxidative Stress in Neurodegeneration (2012, background): “AD brains also show evidence of ROS mediated-injury; there is an increase in levels of malondyaldehyde and 4-hydroxynonenal in brain and cerebrospinal fluid of AD patients compared to controls [6].”
Pathogenic Lysosomal Depletion in Parkinson's Disease (2010, background): “…accumulation of undegraded AP, which may be further enhanced by new AP formation in this pathological situation, in agreement with the known effects of mitochondrial dysfunction and ROS on autophagy induction (Scherz-Shouval and Elazar, 2007; Narendra et al., 2008; Vives-Bauza et al., 2010).”
Etiology and pathogenesis of Parkinson's disease (2011, background): “Studies have also demonstrated mitochondrial dysfunction in patients with the PINK1 mutation.(55,56) Recent studies have demonstrated that PINK1 together with parkin play a vital role in the turnover of mitochondria by autophagy (mitophagy).”