>90%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
<0.10 EU per 1 μg of the protein by the LAL method.
Measured by its ability to inhibit Type-I IFN-mediated anti-viral activity. Symons, J.A. et al. (1995) Cell 81:551. The ED50 for this effect, as measured by inhibition of Recombinant Human IFN‑ alpha 2 (Catalog # 11105-1)
, is 0.3-1.8 ng/mL.
Human embryonic kidney cell, HEK293-derived viral B18R protein
Formulation Lyophilized from a 0.2 μm filtered solution in PBS.
Reconstitution Reconstitute at 250 μg/mL in PBS.
Shipping The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage:Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
B18R (Soluble interferon alpha/beta receptor B18) is a 60-65 kDa protein encoded by the Vaccinia virus genome and by the genomes of other orthopoxviruses. Its function represents one of several mechanisms used by these viruses to evade the host immune response (1, 2). It is known as B18R in the Western Reserve (WR) strain of Vaccinia but as B19R in the Copenhagen strain (3). There is a structurally-unrelated, larger Vaccinia protein that is also known as B18R (or B16R) that contains multiple ankyrin-like repeats (4). The soluble interferon receptor B18R, however, contains three immunoglobulin-like domains and shows homology to human, mouse, and bovine type I interferon receptors (5). The Wyeth strain of Vaccinia virus encodes a truncated protein that lacks the C-terminal Ig-like domain, and B18R is functionally absent in the Lister strain (6, 7). B18R functions as a decoy receptor for type I interferons (IFN alpha, beta, omega). It binds to type I interferons from multiple species and prevents IFN signaling through its receptors (6-8). B18R binds to the surface of virus infected and uninfected cells where it retains its capacity to bind and neutralize IFN (6, 8). It shields those cells from the antiviral effects of type I interferons, thereby enabling virus replication and pathogenicity (6-8). B18R also limits the effectiveness of IFN alpha produced following TLR activation (9), and it limits adaptive T cell responses (3).
Smith, G.L. et al. (2013) J. Gen. Virol. 94:2367.
Perdiguero, B. and M. Esteban (2009) J. Interferon Cytokine Res. 29:581.
Gomez, C.E. et al. (2012) J. Virol. 86:5026.
Goebel, S.J. et al. (1990) Virology 179:247.
Smith, G.L. and Y.S. Chan (1991) J. Gen. Virol. 72:511.
Alcami, A. et al. (2000) J. Virol. 74:11230.
Symons, J.A. et al. (1995) Cell 81:551.
Colamonici, O.R. et al. (1995) J. Biol. Chem. 270:15974.
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