B18R Recombinant Protein Carrier-Free

Also known as: Vaccinia Virus-Encoded Neutralizing Type I Interferon Receptor; Type I IFN inhibitor

RUO: For Research Use Only. Not for use in diagnostic procedures.

SKU# 34-8185

Cat. No. Size
34-8185-81 50 ug
34-8185-85 500 ug
34-8185-86 1 mg

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Data for B18R Recombinant Protein Carrier-Free.

Description

Description: TThe B18R protein is a vaccinia virus-encoded receptor with specificity for mouse, human, rabbit, pig, rat, and cow type I interferons which has potent neutralizing activity. B18R that acts as a decoy receptor for Type I Interferons (IFNa, IFNb, IFNe,k,t,d,z,w,v) . B18R was recently identified to enable increased cell viability during RNA transfection protocols designed to convert human somatic donor cells into iPSCs via direct delivery of modified synthetic mRNAs for OCT4, SOX2, KLF4 and MYC (OSKM) and Lin28 with the aim to enable highly efficient reprogramming of somatic cells to pluripotency. This allows for re-directed differentiation toward a desired lineage while removing the risk of genomic integration and insertional mutagenesis inherent to DNA-bases methodologies and eliminates the need for virus-based approaches. iPSCs represent a widely available, non-controversial and practically infinite source of pluripotent cells.
The B18R protein is a type I interferon receptor encoded by the B18R gene of the Western Reserve vaccinia virus strain. The 60-65 kD glycoprotein is related to the interleukin-1 receptors and is a member of the immunoglobulin superfamily, unlike other type I IFN-receptors, which belong to the class II cytokine receptor family. The B18R protein has a high affinity (KD, 174 pM) for human IFN alpha and, unlike other type I IFN receptors, has broad species specificity, binding to type I interferons of human, mouse, rat, rabbit, pig, and cow. Among viral host response modifiers, the B18R protein is unique in that it exists as a soluble extracellular, as well as a cell surface protein, enabling blockage of both autocrine and paracrine IFN functions. The B18R protein has been shown to inhibit the antiviral potency of IFN-alpha1, IFN-alpha2 , IFN-alpha-8/1/8, and IFN-omega on human cells. The soluble B18R protein is highly potent for neutralizing type I interferons, which include IFN-alpha, beta, delta, kappa. Please note effects on mouse IFNs vary from other species; it has been shown that B18R does not neutralize mouse IFN beta.

Details
Reactivity Bovine, Human, Mouse, Pig, Rabbit, Rat
Purity Greater than 98%, as determined by SDS-PAGE.
Molecular Mass The polypeptide has a predicted molecular mass of 38,389. The DTT-reduced protein migrates as a 48 kDa polypeptide on SDS-PAGE due to glycosylation. The non-reduced protein migrates as a 46 kDa polypeptide on SDS-PAGE due to internal cystines.
Reported Applications Cytokine Bioassays, Cell Culture
Documentation

For complete product information, please download the TDS or IFU document.

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Additional Formats
Cat. No. Name Excite Emit Application Reg.
14-8185 B18R Recombinant Protein FA RUO
References

References: Warren, L. et al. 2010. High efficient reprogramming to pluripotency and directed differentiation of human cells with synthetic modified mRNA. Cell Stem Cell. 7: 618-630.
Symons, J., et al. 1995. Vaccinia virus encodes a soluble type I interferon receptor of novel structure and broad species specificity. Cell. 81: 551-560.
Colamonici, O., et al. 1995. Vaccinia virus B18R gene encodes a type I interferon-binding protein that blocks interferon alpha transmembrane signaling. J. Biol. Chem. 270: 15974 – 15978.
Vancova, I., et al. 1998. Vaccinia virus protein B18R inhibits the activity and cellular binding of the novel type interferon-delta. J. General Virol. 79: 1647-169.
Nagai, T., et al. 2003. Timing of IFN-beta exposure during human dendritic cell maturation and naïve Th cell stimulation has contrasting effects on Th1 subset generation: a role for IFN-beta-mediated regulation of IL-12 family cytokines and IL-18 in naïve Th cell differentiation. J. Immunol. 171: 5233-43. [Bioassay]
Meyers JA, et al. 2006. Blockade of TLR9 agonist-induced type I interferons promotes inflammatory cytokine IFN-gamma and IL-17 secretion by activated human PBMC. Cytokine. 35: 235-46. (B18R, BA PubMed)