The development of inflammatory immune response is related to an activation of nuclear
factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling. The intracellular molecules
from this pathway are sensitive to the alterations in the microenvironment. The changes in cellular redox
state, proliferation, gene expression pattern and genomic stability during inflammation induce the
activation of non-canonical and atypical NK-κB signaling increasing the crosstalk with molecules involved
in neddylation, cell cycle checkpoints regulation and DNA repair. This review article describes
the reactive oxygen species (ROS)-sensitive kinases from the NF-κB pathway and presents the effects of their suppression
by small kinase inhibitors. It illustrates that selective targeting of the redox sensor molecules from the inflammatory NK-
κB cascades can influence cell survival and metabolism as well. We think that this issue is important when evaluating the
drug efficacy in clinical studies and their side effects.
Keywords: Ataxia-telangiectasia (A-T) mutated kinase, IκB kinase, Neddylation, NF-κB pathway, Reactive oxygen species,
Redox sensors, Small molecule inhibitors.
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