Bidirectional regulation of NF-κB by reactive oxygen species: A role of unfolded protein response

Modulation of LPS-induced ROS production and NF-?B nuclear translocation by N-stearoylethanolamine in macrophages

“…It is known that LPS is also a potent activator of NF-κB pathways [11]. In activated cells, phosphorylation of IkB leads to ubiquitination and degradation, allowing free NF-κB complex to translocate to the nucleus where it binds to DNA and induces activation of inflammatory response [12].…”

“…Oxidative stress followed by ROS generation regulate NF-κB activity in a bidirectional fashion, namely, ROS may trigger activation of NF-κB or repress its activity [11]. The opposite, bidirectional effects seem to be phase (early and late)-dependent and context (stimuli and stimulation pattern)-dependent.…”

Rho GTPases, oxidation, and cell redox control

“…[113][114][115] Although the majority of the experimental evidence argues for an activating role of ROS, mostly H 2 O 2 , on NFκB, inhibition of basal NFκB activity by cadmium, a heavy metal that leads to rapid and transient ROS generation, has also been reported. 113 Interestingly, depending on the cellular context, NFκB reciprocally regulates ROS in a bidirectional manner (Fig. 3).…”

Hypoxia/Reoxygenation modulates Oxidative Stress Level and Antioxidative Potential in Lung Mitochondria: Possible participation of P53 and NF-KB Target Proteins

“…It is known, that under resting conditions, NF-B is bound to its co-repressor molecule IB in the cytosol. Upon stimulation, like intermittent hypoxia, IB is degraded and allows p50 and p65 to form NF-B heterodimer, which then translocates to the nucleus and activates transcription of target genes, such as infl ammatory factors and prosurvival proteins [15]. The NF-kB activation is provided by a series of redox-sensitive protein kinases that promote the dissociation of the IkB-NF-kB complex by phosphorylation of either IkB or NF-kB.…”

“…The redox-sensitive transcription factors nuclear factor-kappaB (NF-kB) and p53 are considered as important stress sensors playing crucial role in determining cellular fate during oxidative stress [1,14,15]. Current data have showed that hyper-physiological and physiological levels of p53 exert different effects on cellular redox status either through directly regulating the expression of pro-oxidant and antioxidant genes or through modulating the cellular metabolic pathways [16,17].…”