DJ‐1 has a role in antioxidative stress to prevent cell death

By T. Taira, Yoshiro Saito, T. Niki, Sanae M.M. Iguchi-Ariga, Kazuhiko Takahashi, H. Ariga. EMBO Reports, 2004

890 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/39184000da91b0ea1cdcf12c9798955009855ba6

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. Valina L. Dawson
2. T. Dawson
3. M. Mouradian
4. V. Dias
5. E. Junn
6. M. Beal
7. Christian Haass
8. R. Schwarzenbacher

In Neurology

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

Citations in the corpus

• Molecular pathways to neurodegeneration (2004, background): “DJ-1 is implicated in multiple processes, including oncogenic transformation, gene expression, mRNA sorting and chaperone activit”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “Importantly, this cysteine residue is essential for the stress-protective activity of DJ-1 (Canet-Aviles et al , 2004; Taira et al , 2004; Meulener et al , 2006; Blackinton et al , 2009).”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “On the other hand, knocking down DJ-1 exacerbates the cell death induced by oxidative stress, as well as in response to other insults such as endoplasmic reticulum (ER) stress, proteasome inhibition and calcium entry [342, 348, 349].”
• Epidemiology and etiology of Parkinson’s disease: a review of the evidence (2011, neutral): “scavenger [243].”
• Mitochondrial Dysfunction in Parkinson's Disease (2011, background): “Reports have shown that DJ-1 is present in mitochondria and protects against oxidative neuronal death [103], DJ-1 deficient mice are more susceptible to MPTP [81] and DJ-1 knockdown in a neuroblastoma cell line renders the cells vulnerable to oxidative stress [104].”
• Molecular pathophysiology of Parkinson's disease. (2005, background): “Other missense mutations may similarly reduce the ability of DJ-1 to protect against selective forms of oxidative stress (Takahashi-Niki et al. 2004), and such mutations also share the capacity to reduce DJ1 dimerization (Moore et al.”
• Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “DJ-1 can become oxidized at its cysteine residues upon oxidative stress and thus function as a scavenger of ROS [176].”
• DJ-1 Is a Redox-Dependent Molecular Chaperone That Inhibits α-Synuclein Aggregate Formation (2004, background): “Taira et al. (2004) Open access, freely available online PL o S BIOLOGY recently reported that purified DJ-1 harbors catalase activity, and that overexpression of DJ-1 by transfection of neuroblastoma tumor cells inhibits the accumulation of ROS.”
• Mitochondria take center stage in aging and neurodegeneration (2005, background): “Mutations in the protein render cells more vulnerable to oxidative damage.(57,58) Oxidation of wild-type DJ-1 results in its relocalization to mitochondria where it blocks cell death produced by paraquat and MPP .”