Vangl2 suppresses nf-κb signaling and ameliorates sepsis by targeting p65 for ndp52-mediated autophagic degradation

HIGHLIGHTS

• What: The authors report that is upregulated in patients with sepsis and identify as a negative regulator of NF-κB signaling by regulating the protein stability and activation of the core transcription component p65. The authors provided direct evidence that the expression of Vangl2 was increased during sepsis and upregulated significantly in immune organs (lymph nodes and spleen) upon LPS stimulation, which is consistent with the previous finding that Vangl2 regulated the downstream signaling of TLR or IL-1R. This study showed that Vangl2 prevented the progression of sepsis and the accumulation of inflammatory cytokines through suppressing . . .
  

   

  

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