Crosstalk of reactive oxygen species and NF-κB signaling

By M. Morgan, Zheng-Gang Liu. Cell Research, 2011

3,168 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Toxicology

View Paper: https://www.semanticscholar.org/paper/e8c523d74655e7fb6ecd47c64c487a07289e6f05

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Citations in the corpus

Mitochondria are required for antigen-specific T cell activation through reactive oxygen species signaling (2013, positive): “Multiple reports also suggest Mitochondrial ROS Regulate T Cell Activation that NF-kB requires ROS for activation (Morgan and Liu, 2011); however, phosphorylation of IkB appeared normal in the Uqcrfs1 / T cells (Figure S4G).”
Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements (2019, background): “Elevated ROS levels, accompanied with down-regulation of cellular antioxidant enzyme systems, result in malignant transformation via different molecular targets, such as NF-κB and nuclear factor (erythroid-derived 2)-like-2 factor (Nrf2) [5,6].”
Microbiota in health and diseases (2022, background): “While high ROS level usually results in cell damage, NF-κB pathway is known to promote cell proliferation.(323) Therefore, it is likely that deoxycholic acid can induce cytotoxicity by promoting the generation of ROS, and simultaneously activates NF-κB pathway to allow damaged cells to resist apopto”
Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal (2014, neutral): “Mario F. Muñoz was supported by Consejeria de Economı́a, Innovacion y Ciencia de la Junta de Andalucia (Spain) postdoctoral fellowship (P10-CTS-6494).”
The complexity of NF-κB signaling in inflammation and cancer (2013, background): “Several target genes of NF-κB are involved in the de-toxification of ROS but some of them that can also have a pro-oxidant function such as nitric oxid synthases (NOS) pointing at a complex interplay between ROS and NF-κB [143].”
Reactive oxygen species and mitochondria: A nexus of cellular homeostasis (2015, background): “This inhibition is presumably due to a requirement for ROS in NF-κB activation [2].”
NF-κB in Oxidative Stress (2017, background): “Other reported anti-oxidant targets induced by NF-κB include Glutathione Stransferase pi, Metallothionein-3, NAD(P)H dehydrogenase [quinone]1, heme oxygenase-1 and glutathione peroxidase-1 [37].”
Oxidative Stress in Cancer (2020, background): “However, as NF-κB regulates expression of the pro-oxidant genes CYP2E1, NOX2, XOR, NOS2, COX2, ALOX5, and ALOX12 (Morgan and Liu, 2011; (http://www.bu.edu/nf-kb/gene-resourses/ target-genes/) it may contribute little to adaptation to oxidative stress.”
ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases (2016, background): “Receptor-dependent or nondependent tyrosine kinases, AMP-activated protein kinases, adaptor protein p66SHC, and transcription factors as FOXO (forkhead homeobox type O), Nrf2 (nuclear factor E2-related factor 2), p53 (tumor suppressor 53), NFκB (nuclear factor kappa B), AP-1 (activator protein-1), H”