Each lot of this antibody is quality control tested by ELISA assay. For ELISA capture applications, a concentration range of 4-6 μg/ml is recommended. It is recommended that the reagent be titrated for optimal performance for each application.
Application Notes:
ELISA Capture: The purified JK1RA-1 antibody is useful as the capture antibody in a sandwich ELISA assay, when used in conjunction with the biotinylated Poly5095 (Cat. No. 509501) antibody as the detecting antibody.
Description:
Interleukin-1 receptor antagonist (IL-1RA) is composed of three isoforms, one secreted (sIL-1Rα/IL-1Rα1), two intracellular (IL-1Rα2/IL-1Rα3) and produced by monocytes, tissue macrophages, Langerhans cells, dendritic cells, T and B cells, natural killer (NK) cells, large granular lymphocytes (LGL), vascular endothelium, smooth muscle, fibroblasts, thymic epithelia, astrocytes, microglia, glioma cells, keratinocytes, and chondrocytes. It is upregulated by IL-1β, IL-4, IL-6 and downregulated by glucocorticoids. The JK1RA-1 antibody reacts with human interleukin-1 receptor antagonist (IL-1RA).
Cytokine; three isoforms, one secreted (sIL-1Rα/IL-1Rα1), two intracellular (IL-1Rα2/IL-1Rα3); 17 kD (Mammalian)
Regulation:
Upregulated by IL-1β, IL-4, IL-6; downregulated by glucocorticoids
Cellular Sources:
Monocytes, tissue macrophages, Langerhans cells, dendritic cells, T and B cells, natural killer (NK) cells, large granular lymphocytes (LGL), vascular endothelium, smooth muscle, fibroblasts, thymic epithelia, astrocytes, microglia, glioma cells, keratino
Cellular Targets:
B cells, T cells, monocytes
Receptors:
Type I IL-1R (CDw121a), Type II IL-1R (CDw121b)
Bioactivity/Activities:
Storage forms that are released upon cell death to limit inflammation caused by cell debris; competitive inhibitor of IL-1 receptor binding; antagonizes IL-1 activities without having agonist effects; does not initiate intracellular signal transduction pr
Antigen References:
1. Carter, D., et al., 1990. Nature 344:633. 2. Chirivi, R., et al., 1993. Cancer Res. 53:5051. 3. Holtkamp, G., et al., 1999. Eur. J. Immunol. 29:215. 4. Kim, J., et al., 2003. Gene Ther. 10:1543.
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