Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin

By I. E. Clark, M. Dodson, Changan Jiang, Joseph H. Cao, Jun R. Huh, J. Seol, S. J. Yoo, B. Hay, M. Guo. Nature, 2006

1,812 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/2538f6c34cc4f479463620038fe9cbbcfa186007

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In Cell Biology

1. N. Mizushima
2. Beth Levine
3. V. Deretic
4. Guido Kroemer
5. I. Slaninová
6. D. Klionsky
7. Douglas R. Green
8. Alec C. Kimmelman

In Cellular and Molecular Neuroscience

1. D. C. Chan
2. H. Ko
3. Valina L. Dawson
4. Beth Levine
5. T. Dawson
6. N. Mizushima
7. M. Jäättelä
8. A. Cuervo

In Neurology

1. R. Youle
2. N. Mizushima
3. H. Ko
4. Valina L. Dawson
5. T. Dawson
6. Derek P. Narendra
7. Edward A. Fon
8. H. McBride

Citations in the corpus

• Drosophila orthologues to human disease genes: an update on progress. (2008, background): “In flies, parkin appears to be downstream of pink1 in the same pathway (12, 13).”
• Mitochondria: In Sickness and in Health (2012, background): “Together these proteins collaborate to sense and trigger the removal of ‘‘damaged’’ mitochondria (Clark et al., 2006; Greene et al., 2003; Narendra et al., 2008; Park et al., 2006).”
• Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “Genetic studies in Drosophila suggest that Pink1 and Parkin may function in the same pathway where Pink1 is upstream of Parkin.”
• Oxidative Stress, Mitochondrial Dysfunction, and Aging (2011, background): “A better understanding of response to oxidative stress and mitochondrial dynamics will lead to new therapeutic approaches for the prevention or amelioration of age-associated degenerative diseases.”
• 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].”
• Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin (2010, background): “Proc Natl Acad Sci USA 105(5):1716-1721.”
• The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila (2008, background): “pink15 (10) and parkin25 (13) were previously described.”
• 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.”
• Molecular definitions of autophagy and related processes (2017, positive): “Two physiological settings exem-plify the macroautophagic removal of functional mitochondria: (i) the maturation of reticulocytes and consequent formation of mature erythrocytes, a setting in which mitophagy critically relies on BCL2 interacting protein 3-like (BNIP3L; best known as NIX) and the com”