IL-18R alpha Protein, Mouse, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with His and hFc tag. The predicted molecular weight is 63.5 kDa and the accession number is Q61098.

Mouse

HEK293 Cells

interleukin 18 receptor 1,Il1rrp,Il18rα,Il18ralpha

A DNA sequence encoding the extracellular domain (Met 1-Gly 326) of mouse IL18R1 (NP_032391.1) precursor was fused with the C-terminal polyhistidine-tagged Fc region of human IgG1 at the C-terminus. Predicted N terminal: Lys 20

> 98 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Interleukin-18 receptor 1 (IL18R1) also known as CD218 antigen-like family member A, CDw218a, IL1 receptor-related protein, and CD218a, is an interleukin receptor of the immunoglobulin superfamily. IL18R1 is found expressed in the lung, leukocytes, spleen, liver, thymus, prostate, small intestine, colon, placenta, and heart, and is absent from the brain, skeletal muscle, pancreas, and kidney. A high level of expression is found in Hodgkin disease cell lines. This receptor is specifically bound to interleukin 18 (IL18) and is essential for IL18 mediated signal transduction. IL18R1 contains 3 Ig-like C2-type (immunoglobulin-like) domains and 1 TIR domain. It is a single-pass type I membrane protein. IFN-alpha and IL12 are reported to induce the expression of this receptor in NK and T cells. The increased expression of IL18R1 may contribute pathogenically to disease and is therefore a potential therapeutic target. The absence of a genetic association in the IL18R1 gene itself suggests regulation from other parts of the genome, or as part of the inflammatory cascade in multiple sclerosis without a prime genetic cause.