Figure 1 Self-associated ANGPTL8 regulates NF-kappaB activation

Back to article: A new way to regulate inflammation: selective autophagic degradation of IKKγ mediated by ANGPTL8

FIGURE 1: A negative feedback model of how self-associated ANGPTL8 facilitates autophagic IKKγ degradation. Upon TNFα stimulation, the IKK complexes are formed and activated through the oligomerization of IKKγ (I), to ensure proper NF-κB activation (II). At the same time, inflammatory stimuli such as TNFα induces the up-regulation of ANGPTL8 (AN8, a), then ANGPTL8 and p62 form hetero-oligomers (b), self-association of ANGPTL8 mediates the p62-IKKγ recognition (c); finally, the ANGPTL8-p62-IKKγ complex is degraded in autophagosomes (d). This negative feedback process contributes to the precision control of the NF-κB activation (e).