NRF2 and KEAP1 mutations: permanent activation of an adaptive response in cancer.

By J. Hayes, Michael T. McMahon. TIBS -Trends in Biochemical Sciences. Regular ed, 2009

869 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2c55e816a70d3a1f21cb8d4a5812cc91f3400fb0

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Citations in the corpus

ROS and ROS-Mediated Cellular Signaling (2016, background): “cellular components: Kelch-like ECH-associated protein 1 (Keap1), nuclear factor erythroid 2-related factor 2 (Nrf2), and antioxidant response elements (ARE) [71–76].”
Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease (2015, neutral): “Set against the general role of Nrf2 as an inhibitor of carcinogenesis, it is possibly counterintuitive that somatic mutations resulting in its constitutive activation are a prominent feature of many cancers, a characteristic that is often referred to as the “dark side” of Nrf2 [382] and implies tha”
Role of Glutathione in Cancer Progression and Chemoresistance (2013, background): “Since it is well known that GSH depletion leads to the upregulation of antioxidant genes, many of which are under Nrf2 control and, that in several types of tumors, Nrf2 is constitutively activated [122, 123], a new and indirect approach for cancer therapy may be used to modulate the Nrf2-ARE pathwa”
SCF/β-TrCP Promotes Glycogen Synthase Kinase 3-Dependent Degradation of the Nrf2 Transcription Factor in a Keap1-Independent Manner (2011, background): “Transcription factor Nrf2 (NF-E2-related factor 2) plays a critical role in redox homeostasis as it increases the expression of many antioxidant and drugmetabolizing genes, including heme oxygenase-1 (HO-1), NADPH:quinone oxidoreductase-1, glutathione S-transferases, glutamate-cysteine ligase, and g”
Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “Whereas many aspects of the model are still controversial and the intricate details of the regulation of the pathway are not fully understood (200, 324, 345), there is voluminous experimental evidence for a mechanism of regulation of Keap1 activity through its reactive cysteine residues.”
The Roles of NRF2 in Modulating Cellular Iron Homeostasis (2017, background): “For example, somatic mutations that activate NRF2 or inhibit KEAP1-mediated degradation of NRF2 have shown prevalence in many cancers (40, 138).”
Emerging mechanisms and disease relevance of ferroptosis (2020, background): “Moreover, genomic analyses of human cancers have also uncovered a high frequency of mutations associated with the NRF2–Keap1 axis, validating the bona fide oncogenic role of NRF2 in vivo [55].”
Reactive Oxygen Species in Health and Disease (2012, background): “In patients with T2DM, the form of disease that affects almost 90% of all diabetic patients, some reports have demonstrated a decrease in the copy number of mtDNA in skeletal muscles and in peripheral blood cells [78, 79].”
Oxidative Stress and Air Pollution Exposure (2011, background): “, catalase, superoxide dismutase, and glutathione S-transferase) that counteract ROS formation protecting from adverse biological outcomes [37, 38].”