GITRL, Soluble (mouse, rec.)

The extracellular domain of mouse GITRL (amino acids 45-173) is fused at the N-terminus to a FLAG(R)-tag. Induces GITR-mediated NF-kappaB activation in HEK 293 cells. Liquid. 0.2µm-filtered solution in 10mM glycine, pH 10.0. GITRL (Glucocorticoid-induced TNF receptor ligand) is expressed on dendritic cells (DC), monocytes, macrophages, B cells, activated T cells, endothelial cells, osteoclasts and various healthy non-lymphoid tissues (e.g. testis). GITRL is constitutively expressed and released as soluble form by solid tumors and various hematopoietic malignancies. GITRL causes differentiation of osteoclasts, activation of macrophages, but also alteration of carcinoma and leukemia cells and influences apoptosis. Binding to GITR is important in regulating T cell proliferation and TCR-mediated apoptosis. GITRL is implicated in development of autoimmune diseases and in the immune response against infectious pathogens and tumors.