PMC:7335494 / 5496-6795 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"s, NF-κB (a heterotrimer with p65 and p50 subunits associated with the IκBα inhibitory subunit) is localized to the cytoplasm. Under the effect of inflammatory stimuli (for instance cytokines – IL-8, IL-1β, IL-6, or TNF-α, UV exposure, etc), the heterodimer dissociates, IκBα is degraded, and the two components, p50 and p65, translocate into the nucleus binding the promoter regions from different genes that are involved in initiating several cellular pathways linked to chronic diseases, tumorigenesis, angiogenesis and metastasis. Among the genes regulated by NF-κB are the ones for the expression of TNF-α, COX-2, MMP-9, nitric oxide synthase – the inducible form (iNOS), cytokines (IL-1, IL-6 and IL-8), 5-lipooxigenase (5-LOX), vascular endothelial growth factor (VEGF); all of these genes, when up-regulated fire-up the vicious circle constituted from oxidative stress and inflammation (Aggarwal, 2009; Kawabata et al., 2012; Kunnumakkara et al., 2018; Nimigean et al., 2018, 2019; Poll et al., 2018a, 2018b; Reuter et al., 2010). Interestingly, the NF-κB cascade is also activated by some factors that affect the circadian rhythm, such as aging or sleep deprivation. 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