Protection against electrophile and oxidant stress by induction of the phase 2 response: Fate of cysteines of the Keap1 sensor modified by inducers

By N. Wakabayashi, A. Dinkova-Kostova, W. Holtzclaw, Moon-Il Kang, A. Kobayashi, Masayuki Yamamoto, T. Kensler, P. Talalay. Proceedings of the National Academy of Sciences of the United States of America, 2004

1,014 citations recorded by the source corpus.

Subfields: Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/91b86512938acdbd9738a12407d5b210dedcfeae

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Citations in the corpus

SCF/β-TrCP Promotes Glycogen Synthase Kinase 3-Dependent Degradation of the Nrf2 Transcription Factor in a Keap1-Independent Manner (2011, background): “Failure of Nrf2 to dock simultaneously onto both Kelchrepeat domains enables it to escape ubiquitination by Cul3-Rbx1 (21, 33, 48, 51).”
Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “We and others have reported that C151, C273, and C288 are of particular importance in the function of Keap1 as a sensor for inducers and as a repressor of Nrf2 (154, 253, 461, 477).”
Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022, background): “Dissociation of Nrf2 from Keap1 occurs through the oxidative modification of specific stress-sensing cysteine residues of Keap1 (Figure 6) [55].”
Induction of phase I, II and III drug metabolism/transport by xenobiotics (2005, background): “…et aL recently shown that two of the 15 cysteine residues (Cys273 and Cys288) in Keapl may play an important role in releasing Nrf2 in response to electrophiles and oxidative stress via the formation of an intermolecular disulfide bridge, at least in the test tube (Wakabayashi et aL, 2004).”
The dynamin-related GTPase Drp1 is required for embryonic and brain development in mice (2009, methodology): “After addition of 800 μl Iscove’s modified Dulbecco’s medium (Invitrogen) containing 10% fetal bovine serum (Invitrogen) and 100 μg/ml primocin (Invitrogen), MEFs were dispersed by pipetting (Wakabayashi et al., 2004).”
Mechanistic Studies of the Nrf2-Keap1 Signaling Pathway (2006, background): “The importance of C273 and C288 residues in controlling activation of Nrf2 was confirmed by two other independent groups (Levonen et al., 2004; Wakabayashi et al., 2004).”
The cytoprotective role of the Keap1–Nrf2 pathway (2011, background): “Mutation analysis of the IVR domain showed that substitution of C273 or C288 with either serine or alanine rendered Keap1 unable to repress Nrf2 activity under basal conditions (Zhang and Hannink 2003; Levonen et al. 2004; Wakabayashi et al. 2004).”