Mouse IL18 / IL-18 Protein
Igif,Il-18
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Catalog Number | P50073-MNCE |
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Organism Species | Mouse |
Host | E. coli |
Synonyms | Igif,Il-18 |
Molecular Weight | The recombinant mouse IL18 consists of 158 amino acids and predicts a molecular mass of 18.2 KDa. It migrates as an approximately 19 KDa band in SDS-PAGE under reducing conditions. |
predicted N | Met |
SDS-PAGE | |
Purity | > 90 % as determined by SDS-PAGE |
Protein Construction | A DNA sequence encoding the mouse IL18 (P70380) (Asn36-Ser192) was expressed and purified. |
Bio-activity | Measured by its ability to induce IFN-γ secretion by KG-1 human myelomonocyte. The ED50 for this effect is typically 0.1-0.8 μg/mL. |
Research Area | Cancer |Cancer immunology |Cytokine & Receptor |Interleukin & Receptor |IL-1 family & Receptor |IL-1 family ligand | |
Formulation | Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA. |
Background | Interleukin-18 (IL-18, also known as interferon-gamma inducing factor) is a proinflammatory cytokine that belongs to the IL-1 superfamily and is produced by macrophages and other cells. This cytokine can induce the IFN-gamma production of T cells. The combination of IL-18 and IL12 has been shown to inhibit IL4 dependent IgE and IgG1 production, and enhance IgG2a production of B cells. IL-18 binding protein (IL18BP) can specifically interact with this cytokine, and thus negatively regulate its biological activity. IL-18 is an IL-1−like cytokine that requires cleavage with caspase-1 to become active, was found to increase IgE production in a CD4+ T cells-, IL-4− and STAT6−dependent fashion. IL-18 and T cell receptor−mediated stimulation could induce naïve CD4+ T cells to develop into IL-4−producing cells in vitro. Thus, caspase-1 and IL-18 may be critical in regulation of IgE production in vivo, providing a potential therapeutic target for allergic disorders. IL-18 production in primary synovial cultures and purified synovial fibroblasts was, in turn, upregulated by TNF-α and IL-1β, suggesting that monokine expression can feed back to promote Th1 cell development in synovial membrane. Besides, synergistic combinations of IL-18, IL-12, and IL-15 may be of importance in sustaining both Th1 responses and monokine production in RA. |
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