Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress

By C. Gautier, T. Kitada, Jie Shen. Proceedings of the National Academy of Sciences of the United States of America, 2008

699 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/8a0e30d37ee8099b980ad7ccfef8fdec78bbf45a

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In Epidemiology

1. R. Youle
2. Derek P. Narendra
3. S. Jin
4. Guido Kroemer
5. M. Lazarou
6. D. C. Chan
7. Christian Haass
8. A. Lutz

In Molecular Biology

1. R. Youle
2. D. C. Chan
3. Hsiuchen Chen
4. S. Jin
5. M. Lazarou
6. Derek P. Narendra
7. L. A. Kane
8. D. Suen

In Neurology

1. R. Youle
2. Derek P. Narendra
3. H. Ko
4. S. Jin
5. D. C. Chan
6. M. Lazarou
7. Valina L. Dawson
8. Christian Haass

Citations in the corpus

• Autophagy and aging. (2011, background): “Similarly, mitochondria from the striatum of PINK1 knockout mice are deficient in complexes I and II (Gautier et al., 2008).”
• PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy (2010, neutral): “(PINK1+/+) or PINK1 knockout (PINK1/) mouse (Gautier et al., 2008).”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “Complex I enzymatic activities are reduced in PINK1-deficient mice and flies (Gautier et al , 2008; Morais et al , 2009).”
• Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy. (2010, background): “A progressive inhibition of mitochondrial respiration, accumulation of abnormal mitochondrial morphology and increased oxidative stress have also been reported in two mice PINK1 knockout models (20,22).”
• The Roles of PINK1, Parkin and Mitochondrial Fidelity in Parkinson's Disease (2015, background): “Mitochondria isolated from the striatum or whole brain of aged PINK1-KO mice display defects in complex I (Gautier et al., 2008; Morais et al., 2009), and mitochondria derived from the brains of PINK1-KO mice have reduced calcium-buffering capacity (Akundi et al., 2011).”
• Autophagy and Neurodegeneration: Pathogenic Mechanisms and Therapeutic Opportunities. (2017, positive): “Similarly, deletion of the Pink1 resulted in impaired respiration in striatal mitochondria and increased sensitivity to oxidative stress (Gautier et al., 2008).”
• Mitochondrial dynamics–fusion, fission, movement, and mitophagy–in neurodegenerative diseases (2009, background): “Mitochondria from Pink1 mouse striatal neurons show no gross ultrastructural changes, although a small increase in the number of large mitochondria is observed (50).”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “[151], since mitochondria isolated from the brains of”
• Mitochondrial membrane potential regulates PINK1 import and proteolytic destabilization by PARL (2010, background): “, 2006) linked to mitochondrial maintenance (Greene et al., 2003; Palacino et al., 2004; Gautier et al., 2008).”
• Genetic Animal Models of Parkinson’s Disease (2010, positive): “Similar to parkin knockout mice, PINK1 knockout mice did not exhibit any major abnormality (Table 2) (Gautier et al., 2008; Gispert et al., 2009; Kitada et al., 2007).”
• PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (2010, methodology): “PINK1 and PINK1 primary MEFs were isolated from embryos using a standard protocol [16].”