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.