S-Nitrosylation of Parkin Regulates Ubiquitination and Compromises Parkin's Protective Function

By Kenny K K Chung, B. Thomas, Xiaojie Li, O. Pletnikova, J. Troncoso, L. Marsh, Valina L. Dawson, T. Dawson. Science, 2004

720 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/f52d1ae536120527af84c857f8c2070446ce0f83

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. H. Ko
2. Valina L. Dawson
3. T. Dawson
4. A. Lutz
5. Christian Haass
6. Åsa B. Gustafsson
7. Dieter A. Kubli
8. K. Winklhofer

In Molecular Biology

1. M. Beal
2. Valina L. Dawson
3. T. Dawson
4. M. Mouradian
5. V. Dias
6. E. Junn
7. A. Lutz
8. Michael T. Lin

In Neurology

1. Valina L. Dawson
2. T. Dawson
3. H. Ko
4. D. Selkoe
5. M. Beal
6. Christian Haass
7. A. Lutz
8. K. Winklhofer

Citations in the corpus

• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “Oxidatively modified, misfolded parkin has indeed been found in the brains of PD patients, suggesting that inactivation of parkin may also play a role in sporadic PD (Pawlyk et al , 2003; Chung et al , 2004; Yao et al , 2004; LaVoie et al , 2005; Wang et al , 2005a).”
• Mitochondria take center stage in aging and neurodegeneration (2005, background): “S-nitrosylation of parkin, an oxidative modification, compromises parkin’s ubiquitin ligase function.(54) Genetic studies have also implicated oxidative stress in PD pathogenesis.”
• Molecular pathophysiology of Parkinson's disease. (2005, background): “Because the level of S - nitrosylated proteins is increased in PD and DLB brains in general ( Chung et al .”
• Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “These residues also are susceptible to modification by oxidative and nitrosative stress that lead to Parkin inactivation and aggregation.(161,162) Because cardiac mitochondria are a major source of ROS/reactive nitrogen species during stress, it is likely that aberrant modification of Parkin and sub”
• Molecular pathways to neurodegeneration (2004, background): “New findings indicate that parkin's E3 ligase activity is modified by NO, thus linking environmental stress to a molecular abnormality and a clinical phenotype similar to that seen in hereditary forms of P”
• Genetic Animal Models of Parkinson’s Disease (2010, positive): “Parkin is inactivated by dopaminergic , oxidative, and nitrosative stress, which play key roles in sporadic PD (Chung et al., 2004; LaVoie et al., 2005; Yao et al., 2004).”
• Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases (2006, positive): “S-nitrosylation of parkin, an oxidative modification, impairs its ubiquitin-ligase activity and compromises its protective functio”
• Dopamine covalently modifies and functionally inactivates parkin (2005, background): “Two recent studies found that S -nitrosylation of parkin reduces its E3 ligase activity and that this modification may occur in Parkinson disease brain”
• The physiology and pathophysiology of nitric oxide in the brain. (2005, background): “, in stroke and neurodegenerative diseases (Gu et al., 2002; Chung et al., 2004).”
• Protein S-nitrosylation: purview and parameters (2005, background): “It should be noted that the ubiquitylating activity of at least one E3 ubiquitin ligase, parkin, is regulated directly by S -nitrosylatio”