Keap1/Nrf2 signaling regulates oxidative stress tolerance and lifespan in Drosophila.

By Gerasimos P. Sykiotis, D. Bohmann. Developmental Cell, 2008

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View Paper: https://www.semanticscholar.org/paper/36c563f2d51317b9e3d31dac569b7de85642eaec

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Citations in the corpus

Nrf2:INrf2(Keap1) Signaling in Oxidative Stress (2009, positive): “Nrf2 is ubiquitously expressed in a wide range of tissue and cell types [22] [23] [24] and belongs to a subset of basic leucine zipper genes (bZIP) sharing a conserved structural domain that is designated as a cap'n'collar domain and is highly conserved in Drosophila transcription factor CNC (Fig.”
Stress-Activated Cap’n’collar Transcription Factors in Aging and Human Disease (2010, background): “CncC is also induced by compounds, like oltipraz, that have cancer chemopreventive properties in rodents, and its activation augments the fly’s antioxidant defense systems (155).”
The cytoprotective role of the Keap1–Nrf2 pathway (2011, background): “Nrf2 is conserved in bilaterans with homologues found in nematodes, flies, fish and mammals and was identified due to its ability to bind to NF-E2/AP-1 enhancer elements in cDNA library screens (Moi et al. 1994; Itoh et al. 1995; Kobayashi et al. 2002; An and Blackwell 2003; Sykiotis and Bohmann 200”
Role of nrf2 in oxidative stress and toxicity. (2013, background): “Like Nrf2, CncC dimerizes with a small Maf to activate oxidative defense genes and to resist paraquat and arsenic toxicity (81).”
Role of Nrf2/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism (2016, background): “This mechanism is necessary for transcriptional responses to many xenobiotics, like chlorpromazine, caffeine or the pesticide malathion [29] and represents evolutionarily conserved mechanism of cell adaptations to stressful conditions.”