DJ-1, a cancer- and Parkinson's disease-associated protein, stabilizes the antioxidant transcriptional master regulator Nrf2

By Casey M. Clements, R. S. McNally, Brian J. Conti, T. Mak, J. Ting. Proceedings of the National Academy of Sciences of the United States of America, 2006

824 citations recorded by the source corpus.

Subfields: Molecular Biology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/48b0226f80935e5e62c59b320a8ac03f7b9266d9

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In Molecular Biology

1. A. Abramov
2. A. Dinkova-Kostova
3. I. Harris
4. M. Mouradian
5. Xiongwei Zhu
6. V. Dias
7. Xinglong Wang
8. M. H. Yan

Citations in the corpus

• Molecular Mechanisms of Nrf2-Mediated Antioxidant Response (2009, neutral): “Recently, a cancer and Parkinson's disease associated protein called DJ-1/PARK7 was found to be able to stabilize Nrf2 via preventing Keap1 binding [96].”
• Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “DJ-1 also stabilizes the antioxidant transcriptional master regulator Nrf2 to boost antioxidant response [177].”
• Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, neutral): “Interestingly, the Parkinson-associated protein PARK7/ DJ-1 has been reported to stimulate Nrf2 activity [301], and loss of PARK7/DJ-1 appears to diminish Nrf2 activity [302].”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “Another proposed mechanism for the antioxidant function of DJ-1 is through the stabilization of Nrf2 by preventing the association of this transcription regulator with its inhibitor Keap1 [380].”
• Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022, background): “In both primary human cells and mice, loss of DJ-1 leads to deficits in the expression of Nrf2-mediated stress response enzymes, particularly the detoxification enzyme NQO1, suggesting that DJ-1 is required for Nrf2 stability and Nrf2-mediated transcription [81].”
• Role of nrf2 in oxidative stress and toxicity. (2013, background): “As in neuronal cells, DJ-1 stabilizes Nrf2 by inhibiting Nrf2-Keap1 binding to upregulate cytoprotective genes in cancer cells (72).”
• Regulation of cancer cell metabolism (2011, background): “Similar to p21, DJ1 stabilizes NRF2 and thereby promotes antioxidant response”
• The emerging role of Nrf2 in mitochondrial function (2015, background): “In addition, the mitochondrial protein DJ-1, which plays a role in the maintenance of the activity of complex I [44], has been reported to stabilize Nrf2 [45,46], although the neuroprotective effects of pharmacological or genetic activation of Nrf2 are independent of DJ-1 [47].”
• Nrf2 as a Master Redox Switch in Turning on the Cellular Signaling Involved in the Induction of Cytoprotective Genes by Some Chemopreventive Phytochemicals (2008, neutral): “According According to this study, DJ-1/PARK7 (a cancer and Parkinson' ′ s disease-associated protein) inhibits Nrf2-Keap1 binding and is indispensable for Nrf2 stabilization and subsequent NQO1 induction [43].”
• Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “…of Nrf2 and the sensor for inducers of Nrf2-dependent genes, DJ-1 has been recently implicated as a necessary factor required for Nrf2 stability and activity (130), even though up to date no evidence for a physical interaction between DJ-1 and either Nrf2, Keap1, or Cullin 3 has been reported.”