Plays an essential role in the innate immune defense against viruses and bacteria (PubMed:30150992, PubMed:32404352). Facilitates the type I IFN response by interacting with MAVS at the outer mitochondria membrane and thereby recruiting NF-kappa-B essential modulator IKBKG/NEMO to the MAVS signalosome, leading to the activation of both the IFN regulatory factor 3/IRF3 and NF-kappa-B pathways (PubMed:24379373). Positively regulates the CGAS-induced type I interferon signaling pathway by stabilizing CGAS and inhibiting its autophagic degradation (PubMed:27666593). Acts as a scaffold between TBK1 and STAT3 to promote phosphorylation of STAT3 and resolve interferon-stimulated gene (ISG) expression (PubMed:32404352). Inhibits the transcriptional activity of SPI1 in a dose-dependent manner (By similarity). Interacts with MAVS (PubMed:24379373). Interacts with WRNIP1 and PPP6C; these interactions positively regulate the RIG-I/DDX58 signaling pathway (PubMed:29053956). Interacts with CGAS; this interaction stabilizes CGAS and promotes type I interferon production (PubMed:27666593, PubMed:32404352). Interacts with USP14; this interaction mediates the cleavage of 'Lys-48'-linked ubiquitination of CGAS (PubMed:27666593). Interacts with TBK1 (PubMed:32404352). Interacts with SPI1 (By similarity). (Microbial infection) Interacts with hepatitis B virus HBX; this interaction inhibits formation of the HBX-DDB1 complex, thus inhibiting viral replication. Highest expression in liver; undetectable in skeletal muscle. By interferons alpha and gamma in a STAT1-dependent way. The B-box zinc finger is responsible for inhibition of SPI1-mediated transcriptional activation. Ubiquitinated (PubMed:24379373). Undergoes 'Lys-63'-linked polyubiquitination; this modification allows IKBKG/NEMO recruitment to MAVS. Undergoes 'Lys-48'-linked polyubiquitination by RNF125; this modification mediates its degradation via the ubiquitin-proteasome pathway (PubMed:28476934). Belongs to the TRIM/RBCC family.