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. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Free Radic Biol Med. 2016 May 3;100:108–122. doi: 10.1016/j.freeradbiomed.2016.04.200

Fig. 5. NFκB signaling in the inflammatory response.

Fig. 5

NFκB activation, and subsequent translocation to the nucleus can be initiated by different PAMPs or DAMPs via the toll-like receptors (e.g., TLR4). Mitochondrial H2O2 can facilitate NFκB activation by modulating the redox sensitive Syk and IKK pathways which phosphorylate the inhibitory protein IκB and lead to IκB ubiquitination and degradation, thereby releasing NFκB and its translocation to the nucleus.