Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway.

By T. Kensler, N. Wakabayashi, Shyam Biswal. Annual Review of Pharmacology and Toxicology, 2007

3,601 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b36f22ba2dc5a9f9523d2780d0838daeb6cb6fcb

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Citations in the corpus

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms (2013, background): “inflammatory stresses and chronic exposures to cigarette smoke and other carcinogens [154].”
An Overview of Nrf2 Signaling Pathway and Its Role in Inflammation (2020, positive): “In response to oxidative stress, Nrf2 translocates to the nucleus and activates the transcription of several antioxidant genes, such as glutathione biosynthetic enzymes (GCLM and GCLC), GSH-dependent antioxidant enzymes (glutathione peroxidase 2, GPX2), and glutathione S-transferases (GST) [94].”
Chronic Glutamate Toxicity in Neurodegenerative Diseases—What is the Evidence? (2015, background): “Of note, Cef has been shown not only to induce EAAT2 expression but also to activate the transcription factor Nrf2 (Lewerenz et al., 2009), which induces the transcription of a plethora of genes involved in cytoprotection and antioxidant defense (Kensler et al., 2007).”
Transcriptional control of the inflammatory response (2009, background): “; and several stress-induced transcriptional regulators (such as N -ethylmaleimide-sensitive factor 2 for cellular stress induced by reactive oxygen specie”
Oxidative Stress in Aging Human Skin (2015, background): “Other redox sensitive “switches” are transcription factors such as AP-1, NF- B, NF-E2 related factor-1 (Nfr1), NF-E2 related factor-2 (Nrf2) and Egr1 (early growth response 1) [306,321,322] that modulate gene expression [298] which”
Oxidative Stress and Oxidative Damage in Carcinogenesis (2010, background): “Under basal unstressed conditions, Keap1 (Kelch ECH associating protein 1), a cytosolic Nrf2 repressor protein, binds to Nrf2 and promotes its proteasomal degradation through Cullin 3 (Cul-3)–based E3 ligase (Cullinan et al. 2004).”
When NRF2 Talks, Who's Listening? (2010, positive): “Carcinogenesis, chronic obstructive pulmonary disease, obesogenesis, and neurodegeneration are known to be affected by the Nrf2 genotype in murine models (73).”
Aflatoxin: a 50-year odyssey of mechanistic and translational toxicology. (2011, background): “Inducers disrupt this process, allowing Nrf2 to accumulate and translocate to the nucleus (Kensler et al., 2007).”
The Roles of NRF2 in Modulating Cellular Iron Homeostasis (2017, background): “Many reviews have focused on NRF2-mediated cytoprotection as well as KEAP1 and non-KEAP1-mediated NRF2 activation (34, 38, 56, 58, 86, 171).”
GLUTATHIONE SYNTHESIS (2012, background): “Under non-stressful physiological condition, Nrf2 is kept in the cytosol by Keap1, a component of an E3 ubiquitin ligase complex that targets Nrf2 for proteasomal degradation [110,111].”
Direct interaction between Nrf2 and p21(Cip1/WAF1) upregulates the Nrf2-mediated antioxidant response. (2009, background): “…of an intracellular antioxidant response through transcriptional activation of an array of genes, including phase II detoxifying enzymes, antioxidants, and transporters that protect cells from toxic and carcinogenic chemicals (Kensler et al., 2007; Kobayashi and Yamamoto, 2005; Zhang, 2006).”
The Antioxidant Defense System Keap1-Nrf2 Comprises a Multiple Sensing Mechanism for Responding to a Wide Range of Chemical Compounds (2008, background): “Nrf2 is a transcription factor that transactivates cytoprotective genes through a common DNA regulatory element, called the antioxidant response element or electrophile response element (18, 24).”