Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis.

By R. Thimmulappa, Hannah Lee, T. Rangasamy, S. Reddy, Masayuki Yamamoto, T. Kensler, Shyam Biswal. Journal of Clinical Investigation, 2006

1,045 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/12757d3330912e59469eaada5c7a1ca10ba0e74c

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Citations in the corpus

Global mapping of binding sites for Nrf2 identifies novel targets in cell survival response through ChIP-Seq profiling and network analysis (2010, methodology): “Murine Genome MOE 430A GeneChip arrays (Affymetrix, Santa Clara, CA), which contain probes for detecting 14 500 well-characterized genes and 4371 expressed sequence tags (ESTs) were used to probe the RNA obtained from the cells using the procedure described previously (10).”
NRF2, a Transcription Factor for Stress Response and Beyond (2020, background): “Nfe2l2-deficient mice are hypersensitive to septic shock [120], display more severe lung inflammation induced by cigarette smoke [121], are highly susceptible in different liver inflammation models [122].”
GLUTATHIONE SYNTHESIS (2012, background): “Specifically, LPS-induced mortality and TNFα secretion were higher when GSH level was reduced [162].”
Nrf2, the Master Regulator of Anti-Oxidative Responses (2017, background): “In line with this role, in a murine acute inflammation setting, Nrf2 knockout significantly exacerbated the condition [33], favouring the development of autoimmunity [34].”
NF-κB in Oxidative Stress (2017, background): “Nrf2 knockout cells show more pronounced NFκB activity and enhanced IKK-β function [27] [28].”
ROS Function in Redox Signaling and Oxidative Stress (2014, background): “responses to pathogens, resulting in worsened pneumonia and sepsis [102].”
Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription (2016, methodology): “The binding of p65 was upregulated in LPS-treated cells at the p65-binding sites proximal to IL6 (8) and IL1b (9, 10), similarly to the 60 kb upstream site of the IL6 gene (6) used as a positive control.”
When NRF2 Talks, Who's Listening? (2010, neutral): “CO can repress the formation of TNF-a, IL-1b, and macrophage inflammatory protein-1b and increase IL-10 after LPS stimulation (110).”
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): “Inflammatory responses are exacerbated in the absence of Nrf2—In addition to being susceptible to acute chemical toxicity, Nrf2−/− mice are more susceptible to the proinflammatory effects of allergens, lipopolysaccharide, and a high-fat diet [162, 183, 184].”