Interferon-inducible antiviral protein which plays a major role in the cell antiviral state induced by type I and type II interferon. Catalyzes the conversion of cytidine triphosphate (CTP) to 3'-deoxy-3',4'-didehydro-CTP (ddhCTP) via a SAM-dependent radical mechanism. In turn, ddhCTP acts as a chain terminator for the RNA-dependent RNA polymerases from multiple viruses and directly inhibits viral replication. Therefore, inhibits a wide range of DNA and RNA viruses (PubMed:32719955, PubMed:31517388). Promotes also TLR7 and TLR9-dependent production of IFN-beta production in plasmacytoid dendritic cells (pDCs) by facilitating 'Lys-63'-linked ubiquitination of IRAK1 by TRAF6. Plays a role in CD4+ T-cells activation and differentiation. Facilitates T-cell receptor (TCR)-mediated GATA3 activation and optimal T-helper 2 (Th2) cytokine production by modulating NFKB1 and JUNB activities. Can inhibit secretion of soluble proteins (By similarity). AH2 + CTP + S-adenosyl-L-methionine = 3'-deoxy-3',4'-didehydro-CTP + 5'-deoxyadenosine + A + H(+) + H2O + L-methionine Binds 1 [4Fe-4S] cluster. The cluster is coordinated with 3 cysteines and an exchangeable S-adenosyl-L-methionine. IRAK1 and TRAF6 synergistically activate RSAD2 increasing its activity with CTP as substrate about 10-fold. Homodimer. Interacts with IRAK1 and TRAF6. Interacts with FPPS. Interacts with HADHB. Interacts (via C-terminus) with VAPA/VAP33 (via C-terminus). By interferon type I, type II and LPS. The N-terminal region (1-42) is necessary for its localization to the endoplasmic reticulum membrane and lipid droplet. Acetylated by HAT1. HAT1-mediated acetylation of Lys-198 in turn recruits UBE4A that stimulates RSAD2 polyubiquitination leading to proteasomal degradation. 'Lys-6'-linked polyubiquitination at Lys-207 leads to RSAD2 protein degradation. Belongs to the radical SAM superfamily. RSAD2 family.