Hypersensitivity of DJ-1-deficient mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) and oxidative stress.

By R. H. Kim, Patrice D. Smith, Hossein Aleyasin, S. Hayley, MatthewP . Mount, S. Pownall, A. Wakeham, A. You-Ten, Suneil K. Kalia, P. Horne and 5 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

728 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/541aeebb481c1bdeb90fe03c2afdc3b01f99cb5f

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. M. Mouradian
2. V. Dias
3. Christian Haass
4. E. Junn
5. M. Farrer

In Neurology

1. M. Mouradian
2. V. Dias
3. A. Lutz
4. Christian Haass
5. E. Junn
6. M. Farrer
7. K. Winklhofer
8. Nicole Exner

Citations in the corpus

• Expanding insights of mitochondrial dysfunction in Parkinson's disease (2006, background): “Therefore, loss of DJ1 increases levels of intracellular ROS and increases susceptibility to dopaminergic neuron degeneration in vivo following exposure to exogenous sources of oxidative stres”
• Regulation of cancer cell metabolism (2011, background): “In these disorders, it is believed that loss of DJ1 function leads to elevated oxidative stress in the brain and increased neuronal cell deat”
• Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease (2019, background): “…the accumulation of pathogenic PD‐linked proteins (α‐sy‐ nuclein), deficiency of protective PD‐linked proteins (DJ‐1), or the incorporation of PD‐linked mutations (SNCA) similarly result in ROS‐ dependent apoptosis in cultured human or rat dopaminergic neurons (Kim et al., 2005; Xu et al., 2002).”
• Role of nrf2 in oxidative stress and toxicity. (2013, background): “Loss of DJ-1 leads to early-onset PD in humans; however, DJ-1 KO mice did not show widespread loss of neurons but were more susceptible to neurotoxicant MPTP and oxidative stress (171).”
• Genetics of Parkinson disease: paradigm shifts and future prospects (2006, background): “Primary cultures from DJ1-null mice show increased sensitivity to oxidative stress, whereas overexpression provides a protective effec”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “Similarly to PINK1 and parkin, DJ-1 increases resistance against mitochondrial toxins and decreases mitochondrial fragmentation in response to mitochondrial damage (Canet-Aviles et al , 2004; Kim et al , 2005; Zhang et al , 2005; Irrcher et al , 2010; Krebiehl et al , 2010; Thomas et al , 2011).”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “Conversely, over-expression of DJ-1 in mice ameliorates MPTP-induced nigral neuronal loss [344, 351, 352].”
• Genetic Animal Models of Parkinson’s Disease (2010, neutral): “Some transgenic a-synuclein mice and PINK1 or DJ-1 deficient mice DA neurons are more susceptible to the toxic effects of the DA neurotoxin, MPTP (Haque et al., 2008; Kim et al., 2005; Song et al., 2004).”