GITRL, Soluble (mouse) (rec.)

AdipoGen Life Sciences

GITRL, Soluble (mouse) (rec.)

10

Research Use Only

0.5 mg/ml

>90%

Liquid

Tumor necrosis factor ligand superfamily member 18

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. - Protein. The extracellular domain of mouse GITRL (aa 45-173) is fused at the N-terminus to a FLAG®-tag. Source: HEK 293 cells. Endotoxin content: <0.1EU/microg purified protein (LAL test; Lonza). Liquid. 0.2microm-filtered solution in 10mM glycine, pH 10.0. Binds to mouse GITR. Purity: >90% (SDS-PAGE). 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.

-20°C,2°C to 8°C

12352202