Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin

By Jeehye Park, Sung Bae Lee, Sungkyu Lee, YongSung Kim, Saera Song, Sunhong Kim, E. Bae, Jaeseob Kim, M. Shong, Jin-Man Kim and 1 more. Nature, 2006

1,739 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/43a24e423e29f71eb5903ae9ccaac8ed7529ed7f

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Molecular mechanisms and physiological functions of mitophagy (2021, positive): “Notably, neuron-specific overexpression of Parkin is sufficient to prolong lifespan (Rana et al , 2013), whereas PINK1 mutant flies display shortened lifespan and myopathology (Clark et al , 2006; Park et al , 2006; Yang et al , 2006) .”
The Interplay Between Mitochondrial Dynamics and Mitophagy (2011, background): “The translocation of Parkin is induced by PINK1 (29, 82).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “In ﬂies and cultured cells, parkin can rescue PINK1 deﬁciency but not vice versa , indicating that parkin is acting downstream of PINK1 (Clark et al , 2006; Park et al , 2006; Yang et al , 2006; Exner et al , 2007; Lutz et al , 2009).”
Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase Parkin (2012, background): “In Drosophila, PINK1 and Parkin function in the same pathway to maintain mitochondrial fidelity (Clark et al., 2006; Greene et al., 2003; Park et al., 2006; Yang et al., 2006) supporting prior studies indicating that mitochondrial dysfunction may be a contributing factor in PD (Schapira, 2010).”
FOXO/4E-BP Signaling in Drosophila Muscles Regulates Organism-wide Proteostasis During Aging (2010, methodology): “For transgene expression with the Gal4-UAS system, flies were reared at 25 C. Behavioral and Metabolic Assays Flight ability was scored according to Park et al. (2006), and negative geotaxis assays were performed as previously described (Rhodenizer et al., 2008).”
Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL (2010, background): “…cases of Parkinson’s disease, PINK1 (Valente et al., 2004) and Parkin (Kitada et al., 1998), have been found to work in the same pathway (Clark et al., 2006; Park et al., 2006; Yang et al., 2006) linked to mitochondrial maintenance (Greene et al., 2003; Palacino et al., 2004; Gautier et al., 2008).”
Autophagy as a target for anticancer therapy (2011, background): “Defective mitophagy was linked to Parkinson's disease, as patients with this disease often have mutations in the Parkinson-associated genes PINK1 and PARK2 , which are important for mitophagy induction”
The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “PINK-1 mutant flies share a similar phenotype as parkin mutants [152, 328], and over-expression of parkin can rescue the mitochondrial defects of PINK-1 mutant flies [152, 328, 329].”
PINK1 is activated by mitochondrial membrane potential depolarization and stimulates Parkin E3 ligase activity by phosphorylating Serine 65 (2012, background): “This may explain why over-expression of Parkin in dPINK1 null Drosophila restores ubiquitylation of targets and rescues the null phenotype [4,5].”
PINK1 is degraded through the N-end rule pathway (2013, methodology): “Furthermore, PINK1(1-155)-YFP, a mutant with an N-end stabilizing residue was stably localized in the cytosol (Fig.”
Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy. (2010, background): “PINK1 deficiency in Drosophila also causes loss of mitochondrial integrity and dopaminergic neuronal loss (23,24).”