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ANGPTL8 negatively regulates NF-κB activation by facilitating selective autophagic degradation of IKKγ
Update time:2018-05-24 01:49:36   【 Font: Large  Medium Small

Abstract

Excessive nuclear factor-kB (NF-kB) activation mediated by tumor necrosis factor alpha (TNF alpha) plays a critical role in inflammation. Here we demonstrate that angiopoietin-like 8 (ANGPTL8) functions as a negative feedback regulator in TNF alpha-triggered NF-kB activation intracellularly. Inflammatory stimuli induce ANGPTL8 expression, and knockdown or knockout of ANGPTL8 potentiates TNF alpha-induced NF-kB activation in vitro. Mechanistically, upon TNF alpha stimulation, ANGPTL8 facilitates the interaction of IKK gamma with p62 via forming a complex, thus promoting the selective autophagic degradation of IKK gamma. Furthermore, the N-terminal domain mediated self-oligomerization of ANGPTL8 is essential for IKK gamma degradation and NF-kB activation. In vivo, circulating ANGPTL8 level is high in patients diagnosed with infectious diseases, and the ANGPTL8/p62-IKK gamma axis is responsive to inflammatory stimuli in the liver of LPS-injected mice. Altogether, our study suggests the ANGPTL8/p62-IKK gamma axis as a negative feedback loop that regulates NF-kB activation, and extends the role of selective autophagy in fine-tuned inflammatory responses.

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