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. Author manuscript; available in PMC: 2016 Sep 23.
Published in final edited form as: Nature. 2016 Mar 23;532(7599):394–397. doi: 10.1038/nature17631

Extended Data figure 1. Schematic of ER stress and NOD1/2 signaling.

Extended Data figure 1

(a) Model of how ER stress induces a NOD1/2-dependent pro-inflammatory response through a TUDCA/KIRA6-sensitive pathway, which differs from the TUDCA/KIRA6-resistant pathways induced by bacterial peptidoglycan fragments (MDP or C12-iE-DAP). (b) NF-κB activation induced by ectopic expression of VceC in HEK293 cells transfected with a dominant negative form of TRAF2 or a vector control. (c) NF-κB activation mediated by expression-induced auto-activation of NOD1, NOD2 or RIP2 in HEK293 cells that were transfected with a dominant negative form of TRAF2 or a vector control. Data are expressed as mean luciferase activity ± s.e.m. from five independent experiments.