The PINK1/Parkin pathway regulates mitochondrial morphology

By Angela C. Poole, Ruth E. Thomas, Laurie A. Andrews, H. McBride, Alexander J. Whitworth, L. Pallanck. Proceedings of the National Academy of Sciences of the United States of America, 2008

928 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Epidemiology, Neurology

View Paper: https://www.semanticscholar.org/paper/3480d46322f4c74b4a102f5d5ddc2659a5147b06

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Citations in the corpus

Mechanisms of mitophagy (2011, background): “, which can lead to loss of flight muscle and dopaminergic neurons, and to male sterility that is ameliorated by promotion of mitochondrial fissio”
The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila (2008, background): “In addition, as we have shown, pink1 and parkin mutants show synthetic lethality with a heterozygous mutation in drp1 (26).”
Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin (2010, background): “Interestingly, perturbing mitochondrial dynamics by either promoting fission or suppressing fusion can compensate for pink1 and parkin mutations (Deng et al., 2008; Poole et al., 2008; Yang et al., 2008; Park et al., 2009).”
Mitochondria: In Sickness and in Health (2012, background): “In flies, attenuation of mitochondrial fusion or stimulation of mitochondrial division can rescue phenotypes associated with PINK1 or Parkin mutants, and loss of division exacerbates these phenotypes and causes lethality (Deng et al., 2008; Poole et al., 2008).”
Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin (2010, background): “In particular, that promoting mitochondrial fragmentation, by overexpression of Drp1 or reduction of Mfn and Opa1, is able to partially suppress the locomotor deficits, muscle degeneration and mitochondrial abnormalities (9-12).”
Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins (2008, background): “In this regard, it is worth noting that PINK1, mutations of which lead to Parkinson disease, appears to play a role in mitochondrial fission through regulation of DLP1 (34), and fibroblasts from patients with Parkinson disease bearing PINK1 mutations also exhibit abnormal mitochondrial morphology (3”
Visualizing stromal cell dynamics in different tumor microenvironments by spinning disk confocal microscopy (2008, background): “Interestingly, while the Pink1/Parkin pathway has recently been linked to mitochondrial dynamics (Exner et al., 2007; Poole et al., 2008; Yang et al., 2008) – the process of fission and fusion reactions that control mitochondrial morphology – the function of the mitochondrial rhomboids in yeast, fli”
The pathways of mitophagy for quality control and clearance of mitochondria (2012, background): “Several proteins are now identified that are critical in directing autophagosomes to the mitochondria, including ATG32, Nix, p62, PINK1, and Parkin.”
Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress (2008, neutral): “How can one explain such a protective role of PINK1 in mitochondria? One possibility, raised by studies in flies, is that PINK1 is involved in the regulation of mitochondrial fission and fusion (16, 17).”
PINK1-dependent recruitment of Parkin to mitochondria in mitophagy (2009, background): “Given the reported Parkin/Pink1 genetic interaction observed in Drosophila (4, 5, 7) and our revised PINK1 topology (10), we then asked whether PINK1 plays any role in the mitochondrial recruitment of Parkin.”