Immobilized Biotinylated Human IL-18 RAP, His Avi Tag at 0.5 μg/ml (100 μl/well) on the streptavidin precoated plate (5 μg/ml). Dose response curve for Anti-IL-18RAP Antibody, hFc Tag with the EC50 of 6.4 ng/ml determined by ELISA.

IL-18R beta/IL-18RAP Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with His and Avi tag. The predicted molecular weight is 41.35 kDa and the accession number is O95256-1.

Human

HEK293 Cells

interleukin 18 receptor accessory protein,IL-1RAcPL,IL-1R-7,IL-1R7,IL-18R-β,IL-18Rβ,IL-18R-beta,IL-18Rbeta,IL18RB,IL-18RAcP,IL-18R β/IL-18RAP,CDw218b,CD218b,ACPL

Phe20-Arg356

> 95% as determined by Bis-Tris PAGE; > 95% as determined by HPLC

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 accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand-binding subunit of the IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high-affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the etiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity, and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.