Keap1 regulates both cytoplasmic‐nuclear shuttling and degradation of Nrf2 in response to electrophiles
By K. Itoh, N. Wakabayashi, Y. Katoh, T. Ishii, T. O'connor, Masayuki Yamamoto. Genes to Cells, 2003
852 citations recorded by the source corpus.
Subfields: Cell Biology, Clinical Biochemistry, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d6e5b826f64305470f4a07527604ddcb48e92736
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- Masayuki Yamamoto
- Donna D. Zhang
- A. Dinkova-Kostova
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Citations in the corpus
- Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex (2004, background): “02 g, lanes 2 to 5), and Cul3(1-380) (from 0.”
- Distinct Cysteine Residues in Keap1 Are Required for Keap1-Dependent Ubiquitination of Nrf2 and for Stabilization of Nrf2 by Chemopreventive Agents and Oxidative Stress (2003, background): “Steady-state levels of Nrf2 are increased in cells treated with known inducers of Nrf2-dependent transcription, including oltipraz, tBHQ, sulforaphane, and cadmium (15, 19, 25, 29, 37).”
- Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications. (2006, background): “Keap1 retains Nrf2 in the cytoplasm and promotes its ubiquitination and degradation by the proteosome (274, 332, 436).”
- The cytoprotective role of the Keap1–Nrf2 pathway (2011, background): “…and diethyl maleate (DEM), and each time the inducer was shown to stabilise Nrf2 (Nguyen et al. 2003; McMahon et al. 2003; Itoh et al. 2003), whereas the level of Nrf2 mRNA was unaffected by the addition of inducers (Stewart et al. 2003; Nguyen et al. 2003; McMahon et al. 2003; Itoh et al. 2003).”
- Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “The Kelch-like ECH-associated protein 1 (Keap1) retains Nrf2 in the cytoplasm and promotes its proteosomal degradation under basal condition (192, 193).”
- NRF2, a Transcription Factor for Stress Response and Beyond (2020, background): “As a result, newly synthesized NRF2 accumulates in the nucleus and activates the expression of cytoprotective genes [3,8].”
- The Molecular Mechanisms Regulating the KEAP1-NRF2 Pathway (2020, background): “Importantly, in the absence of protein translation, NRF2 is not stabilized by inducers, which suggests that newly translated NRF2 is required for the upregulation of ARE-dependent gene expression (50, 55).”
- Oxidative and Electrophilic Stresses Activate Nrf2 through Inhibition of Ubiquitination Activity of Keap1 (2006, background): “It has been shown previously that Keap1 binds to Nrf2 and represses its activity (15, 16, 18) and that Keap1 promotes the rapid turnover of Nrf2 through the ubiquitin-proteasome pathway utilizing Cul3based E3 ligase (6, 11, 22, 44).”
- The Antioxidant Defense System Keap1-Nrf2 Comprises a Multiple Sensing Mechanism for Responding to a Wide Range of Chemical Compounds (2008, background): “contains the Neh2 domain, a degron for Keap1-dependent degradation of Nrf2, which has been shown to be functional not only in cultured cells but also in mouse and zebrafish (13, 26).”