Direct evidence that sulfhydryl groups of Keap1 are the sensors regulating induction of phase 2 enzymes that protect against carcinogens and oxidants

By A. Dinkova-Kostova, W. Holtzclaw, R. Cole, K. Itoh, N. Wakabayashi, Y. Katoh, Masayuki Yamamoto, P. Talalay. Proceedings of the National Academy of Sciences of the United States of America, 2002

1,958 citations recorded by the source corpus.

Subfields: Health, Toxicology and Mutagenesis, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/28acd9c174184b3b379bd61e25eaa5209aafd495

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Citations in the corpus

The Nrf2 cell defence pathway: Keap1-dependent and -independent mechanisms of regulation. (2013, background): “AN, xanthohumol [122]; LIQ, liqustilide [126]; P-SS-P, protein disulfide; P-SG, NCB, dinitrochlorobenzene [74]; DEX-MES [65,74]; 15d-PGJ2, 15-deoxy-D12,14-”
Regulation of inflammation and redox signaling by dietary polyphenols. (2006, background): “chemically induced oxidative/electrophilic stress [76] (Fig.”
High glucosinolate broccoli: a delivery system for sulforaphane (2006, background): “…following SF absorption and glutathione depletion, leading to dissociation of the transcription factor Nrf2 with the Keap1 protein, translocation of Nrf2 to the nucleus and its binding to ARE domains in a suit of phase II detoxification genes leading to transcription (Dinkova-Kostova et al. 2002).”
Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex (2004, background): “Talalay and coworkers have identified four cysteine residues in Keap1 (Cys 257, Cys 273, Cys 288, and Cys 297) that are preferentially labeled following in vitro exposure of purified Keap1 to a cysteine-reactive alkylating agent (16, 52).”
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): “Keap1 is a cysteine-rich homodimeric,multi-domain zinc metal-loprotein [36].”
Small Molecule Modulators of Keap1-Nrf2-ARE Pathway as Potential Preventive and Therapeutic Agents (2012, background): “229 D3T and other synthetic substituted derivatives, such as ADT (66) and oltipraz (67), have been shown to induce the expression of cytoprotective genes through the Keap1-Nrf2 signaling pathway.”
p62 links autophagy and Nrf2 signaling. (2015, neutral): “(AREs) in their regulatory regions [3–5] (Fig.”
Redox Regulation of Cell Survival (2008, positive): “7, sulfhydryl modifications dissociate Keap1 from Nrf2, allowing the translocation of Nrf2 to the nucleus, where it transactivates target-gene expression (70).”
Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications. (2006, background): “Keap1 contains critical -SH groups susceptible to oxidation, suggesting that release of Nrf2 by Keap1 is potentially under redox control (143, 374, 613).”
ROS and ROS-Mediated Cellular Signaling (2016, methodology): “Nrf2 for degradation by the 26S proteasome (more related information has been provided in “ROS and Ubiquitination/Proteasome System” section) [78].”
Mechanistic Studies of the Nrf2-Keap1 Signaling Pathway (2006, background): “Identification of Keap1 as the key repressor for Nrf2 leads to the prevailing model that one or more of the 27 cysteine residues in the human Keap1 protein are components of a molecular switch that is triggered by intracellular redox changes (Dinkova-Kostova et al., 2002).”