Facilitator of innate immune signaling that promotes the production of type I interferon (IFN-alpha and IFN-beta). Innate immune response is triggered in response to non-CpG double- stranded DNA from viruses and bacteria delivered to the cytoplasm. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon and exert a potent anti- viral state following expression. May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons. May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II). Mediates death signaling via activation of the extracellular signal-regulated kinase (ERK) pathway. Associates with the MHC-II complex. Homodimer; 'Lys-63'-linked ubiquitination at Lys-150 is required for homodimerization. Interacts with DDX58/RIG-I, MAVS/VISA and SSR2. Interacts with RNF5 and TRIM56. Interacts with TBK1; when homodimer, leading to subsequent production of IFN-beta. Ubiquitously expressed. Belongs to the TMEM173 family. Note: This description may include information from UniProtKB.
Cellular Component: cytoplasmic vesicle membrane; endoplasmic reticulum membrane; mitochondrial outer membrane; perinuclear region of cytoplasm
Molecular Function: identical protein binding; protein binding; protein homodimerization activity; protein kinase binding; transcription factor binding
Biological Process: activation of innate immune response; defense response to virus; innate immune response; interferon-beta production; positive regulation of defense response to virus by host; positive regulation of interferon type I production; positive regulation of protein binding; positive regulation of protein import into nucleus, translocation; positive regulation of transcription factor import into nucleus; positive regulation of transcription from RNA polymerase II promoter; regulation of interferon type I production
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.