Negative feedback regulator that controls excessive innate immune responses. Regulates both Toll-like receptor 4 (TLR4) and DDX58/RIG1-like helicases (RLH) pathways. May inhibit the LTR pathway by direct interaction with TRAF6 and attenuation of NF-kappa-B activation. May negatively regulate the RLH pathway downstream from MAVS and upstream of NF-kappa-B and IRF3. Interacts with MAVS, TICAM1, TRAF1, TRAF2, TRAF3 and TRAF6. Expressed in skeletal muscle, brain, liver, kidney, spleen and bone marrow. Expression depends on STAT1. By lipopolysaccharide (LPS), IFNB1 and IFNG, IFNB1 being most rapid and potent inducer (at protein level). Not induced by anti-inflammatory cytokines, such as IL4 and IL10, which also inhibit LPS induction of TRAFD1. Mice show no gross developmental abnormalities, but exhibit an increased susceptibility to LPS-induced septic shock and are more sensitive to poly(I:C) shock, suffering more severe hepatic damage than wild-type animals. In response to LPS-stimulation, bone marrow-derived dendritic cells display an increased production of pro-inflammatory cytokines, such as IL6, TNF and IL12, as well as elevated IKK and JNK activation, compared to wild-type mice. Mutant embryonic fibroblasts are more resistant to vesicular stomatitis virus (VSV)-induced cytopathic effect.