Anti-IL1 beta

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Interleukin-1 beta (IL-1b) is a potent stimulator of bone resorption whose gene is mapped to 2q14, and has been implicated in the pathogenesis of high bone turnover and osteoporosis. IL-1b, a prominent microglia-derived cytokine, caused oligodendrocyte death in coculture with astrocytes and microglia, but not in pure culture of oligodendrocytes alone. It also can cause nuclear export of a specific NCOR corepressor complex, resulting in derepression of a specific subset of nuclear factor-kappa-B (NFKB)-regulated genes. Furthermore, Microenvironmental IL-1b and, to a lesser extent, IL-1? are required for in vivo angiogenesis and invasiveness of different tumor cells. Additional, the cooperation of IL-1b and PDGFB induces contractile-to-synthetic phenotype modulation of human aortic smooth muscle cells in culture. Moreover, the association with disease may be explained by the biologic properties of IL-1b, which is an important proinflammatory cytokine and a powerful inhibitor of gastric acid secretion. Protein function: Potent pro-inflammatory cytokine. Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B- cell activation and antibody production, and fibroblast proliferation and collagen production. Promotes Th17 differentiation of T-cells. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T- helper 1 (Th1) cells. Plays a role in angiogenesis by inducing VEGF production synergistically with TNF and IL6. Involved in transduction of inflammation downstream of pyroptosis: its mature form is specifically released in the extracellular milieu by passing through the gasdermin-D (GSDMD) pore. [The UniProt Consortium]