Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin.

By Yufeng Yang, S. Gehrke, Y. Imai, Zhinong Huang, Yingshi Ouyang, Ji-Wu Wang, Lichuan Yang, M. Beal, H. Vogel, B. Lu. Proceedings of the National Academy of Sciences of the United States of America, 2006

839 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Epidemiology, Neurology

View Paper: https://www.semanticscholar.org/paper/14f85e478013382aeafe63bc0ead5e9102e9611a

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Citations in the corpus

Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin (2010, background): “Genetic studies in Drosophila show that PINK1, a kinase located in mitochondria, functions upstream of Parkin, an E3 ubiquitin (Ub) ligase located in the cytosol, in the same pathway that preserves mitochondrial integrity (Clark et al., 2006; Park et al., 2006; Yang et al., 2006).”
PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy (2010, background): “…retrieves Parkin from the cytoplasm to the mitochondria Because previous studies revealed that PINK1 functions upstream of Parkin (Clark et al., 2006; Park et al., 2006; Yang et al., 2006; Exner et al., 2007), we next examined the potential role of PINK1 in the mitochondrial recruitment of Parkin.”
A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles (2014, background): “PINK1 and Parkin are both mutated in familial cases of Parkinson’s disease (PD) (Trinh & Farrer, 2013) and were initially shown to act in a common pathway in mitochondrial quality control in Drosophila models of PD (Clark et al, 2006; Park et al, 2006; Yang et al, 2006).”
The Fly as a Model for Neurodegenerative Diseases: Is It Worth the Jump? (2007, positive): “evidence from Drosophila lately added a twist to an emerging pathophysiology of PD. Indeed, several recent studies demonstrate that knockdown [”
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).”
Mitochondrial dynamics–fusion, fission, movement, and mitophagy–in neurodegenerative diseases (2009, background): “These findings have led to the model that Pink1 and Parkin likely act in the same pathway, with Parkin downstream of Pink1 (56,58,59).”
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).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “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).”
Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases (2006, positive): “This pathology resembles that of parkin -mutant flies, and can be rescued by overexpression of parkin, but not DJ-1 (ref”
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) .”
Pink1, Parkin, DJ-1 and mitochondrial dysfunction in Parkinson's disease. (2007, background): “Mitochondria within dopaminergic neurons in pink1 mutants also display aberrant morphology [19 ], and a small but statistically significant loss of a subset of these neurons occurs with age [19 ,20 ,21].”