Molecular Mechanisms of Nrf2-Mediated Antioxidant Response
By Wenge Li, A. Kong. Molecular Carcinogenesis, 2009
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Nrf2 is the key transcription factor regulating the antioxidant response. Nrf2 signaling is repressed by Keap1 at basal condition and induced by oxidative stress. Keap1 is recently identified as a Cullin 3‐dependent substrate adaptor protein. A two‐sites binding “hinge & latch” model vividly depicts how Keap1 can efficiently present Nrf2 as substrate for ubiquitination. Oxidative perturbation can impede Keap1‐mediated Nrf2 ubiquitination but fail to disrupt Nrf2/Keap1 binding. Nrf2 per se is a redox‐sensitive transcription factor. A new Nrf2‐mediated redox signaling model is proposed based on these new discoveries. Free floating Nrf2 protein functions as a redox‐sensitive probe. Keap1 instead functions as a gate keeper to control the availability of Nrf2 probes and thus regulates the overall sensitivity of the redox signaling. © 2008 Wiley‐Liss, Inc.
Subfields: Molecular Biology, Plant Science
View Paper: https://www.semanticscholar.org/paper/46d625fe885a07d1e6c87e83a93ec08ee6c2794b
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Citations in the corpus
- Small Molecule Modulators of Keap1-Nrf2-ARE Pathway as Potential Preventive and Therapeutic Agents (2012, background): “146 Recently, the fluorescein-based biarsenical thiol labeling reagent (FlAsH-EDT2, 74) and phenylarsine oxide (75) were found to produce Keap1-dependent activation of Nrf2.”
- Oxidative Stress and Oxidative Damage in Carcinogenesis (2010, background): “…allele of this SNP was shown to be associated with significantly increased risk of a number of human cancers, including lung (Hung et al. 2005; W. Li and Kong 2008), eso- phageal (Xing et al. 2001), prostate (Xu et al. 2002), and gastric (Farinati et al. 2008) cancer but not with squamous…”