Pink1, Parkin, DJ-1 and mitochondrial dysfunction in Parkinson's disease.
284 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology, Computational Biology & Bioinformatics, Neuroscience
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In Cellular and Molecular Neuroscience
In Molecular Biology
In Neurology
Citations in the corpus
- The Role of Oxidative Stress in Parkinson’s Disease (2013, unknown): “to demonstrate this rescue effect [329, 334].”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “In addition, several of these genes, including parkin, PINK1, DJ-1, and Omi/Htra2 are linked to the mitochondria and may have roles in mitochondrial function and resistance to oxidative stress [254].”
- Human iPSC-based Modeling of Late-Onset Disease via Progerin-induced Aging (2013, unknown): “PINK1 and Parkin are thought to act in a common pathway to promote the autophagic degradation of damaged mitochondria (Dodson and Guo, 2007), in addition to the unique functions of Parkin in the ubiquitin-proteasome pathway (Shimura et al.”
- Oxidative Stress, Mitochondrial Dysfunction, and Aging (2011, background): “Genetic studies of PINK1 and PARKIN further support the role of mitochondrial dysfunction in pathogenesis of PD [179, 180].”
- PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy (2010, background): “PINK1 functions in mitochondrial maintenance, suggesting that mito chondrial integrity is another key factor in disease patho genesis (Dodson and Guo, 2007; Schapira, 2008).”