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. 2014 Aug 1;9(8):e103794. doi: 10.1371/journal.pone.0103794

Figure 1. IL-1/TLR-induced NFκB signaling pathway.

Figure 1

After the stimulation, IL-1R/TLR recruits adaptor molecule myeloid differentiation factor 88(MyD88) to their TIR domain, which further recruits and activates IRAK4. Then IRAK4, TRAF6 and IRAKs combine into a complex. After the coalition of Pellino2 and TAK1, the new complex is divided into at least two parts: complex including TAK1, activating NFκB through IκBα phosphorylation and degradation, and complex including IRAK4 which phosphorylates p38 and binds to the ARE-binding proteins like HuR and c-Myc. Two complexes both promote the release of cytokines and chemokines like IL-6 to further promote inflammation response. During the process EMR1 keeps growing.