RSAD2: Interferon-inducible iron-sulfur (4FE-4S) cluster- binding antiviral protein which plays a major role in the cell antiviral state induced by type I and type II interferon. Can inhibit a wide range of DNA and RNA viruses, including human cytomegalovirus (HCMV), hepatitis C virus (HCV), west Nile virus (WNV), dengue virus, sindbis virus, influenza A virus, sendai virus, vesicular stomatitis virus (VSV), and human immunodeficiency virus (HIV-1). Displays antiviral activity against influenza A virus by inhibiting the budding of the virus from the plasma membrane by disturbing the lipid rafts. This is accomplished, at least in part, through binding and inhibition of the enzyme farnesyl diphospate synthase (FPPS), which is essential for the biosynthesis of isoprenoid-derived lipids. Promotes TLR7 and TLR9-dependent production of IFN-beta production in plasmacytoid dendritic cells (pDCs) by facilitating Lys-63'-linked ubiquitination of IRAK1. 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. Belongs to the radical SAM superfamily. RSAD2 family.
Chromosomal Location of Human Ortholog: 2p25.2
Cellular Component: Golgi apparatus; endoplasmic reticulum membrane; mitochondrial outer membrane; mitochondrion; endoplasmic reticulum; mitochondrial inner membrane; lipid particle
Molecular Function: protein binding; protein self-association; metal ion binding; 4 iron, 4 sulfur cluster binding; catalytic activity
Biological Process: positive regulation of toll-like receptor 7 signaling pathway; ossification; negative regulation of protein secretion; CD4-positive, alpha beta T cell differentiation; viral reproduction; negative regulation of viral genome replication; metabolic process; cytokine and chemokine mediated signaling pathway; response to virus; positive regulation of toll-like receptor 9 signaling pathway; regulation of ossification; defense response to virus
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