An important function of Nrf2 in combating oxidative stress: Detoxification of acetaminophen

By K. Chan, Xiao-dong Han, Y. Kan. Proceedings of the National Academy of Sciences of the United States of America, 2001

786 citations recorded by the source corpus.

Subfields: Molecular Biology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/6c1cada59f1078f05b1769cdd20901ef2ecec243

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In Molecular Biology

1. A. Goldberg
2. Q. Ma
3. S. Lecker
4. W. Mitch
5. T. Blackwell
6. D. Trachootham
7. Donna D. Zhang
8. Peng Huang

In Pharmacology

1. Shelly C. Lu

Citations in the corpus

• Redox Regulation of Cell Survival (2008, positive): “Nrf2 plays a critical role in protection against oxidative damage induced by acute injury, hyperoxia, nitrosative stress, ER stress, and exogenous proox-idative agents (43, 178, 189, 295).”
• The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state (2015, background): “The function of Nrf2 and its downstream proteins has been shown to be important for protection against oxidative/nitrosative stress- or chemical-induced cellular damage in liver [48, 49] and lung [50] as well as for prevention of cancer formation in the gastrointestinal tract [51, 52] and promotion ”
• Role of nrf2 in oxidative stress and toxicity. (2013, background): “Although acetaminophen-induced injury is morphologically similar to necrosis, acetaminophen induces BAX-translocation to mitochondria to increase apoptosis, which is inhibited by Nrf2 (13, 124, 128) (Supplemental Table 1).”
• Idiosyncratic drug hepatotoxicity (2005, background): “Nrf2 −/− mice are more susceptible to APAP toxicit”
• SKN-1 links C. elegans mesendodermal specification to a conserved oxidative stress response. (2003, background): “This gene activation pathway is also important for drug detoxification, and therefore for chemotherapeutic agent tolerance, and it may provide a widely applicable means of cancer prevention (Chan et al. 2001; Hayes and McMahon 2001; Wolf 2001).”
• Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression (2004, background): “expression of oxygen-stress response genes (49, 50),”