Technical Data
GITRL, Soluble, Recombinant, Mouse (His) (Glucocorticoid-induced TNF Receptor Ligand, AITRL, Activation-inducible TNF-related Ligand, TNFSF18)
Molecular Biology Storage: 4C/-20CShipping: Blue Ice
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.

Biological Activity:
Induces GITR-mediated NF-kappaB activation in HEK 293 cells.

The extracellular domain of mouse GITRL (aa 45-173) is fused at the C-terminus to a His-tag.

Storage and Stability:
Short-term Storage: +4C
Long-term Storage: -20C
Working aliquots are stable for up to 3 months when stored at -20C.

Molecular Weight:
~16kD (SDS-PAGE)
Source: Mouse, E. coli
Purity: >90% (SDS-PAGE)
Concentration: 0.5mg/ml
Form: Supplied as a liquid from a 0.2um-filtered solution in 10mM glycine, pH 10.0.
Specificity: Binds to mouse GITR.

Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.
Product Reference: Identification of a ligand for glucocorticoid-induced tumor necrosis factor receptor constitutively expressed in dendritic cells: K.Y. Yu, et al.; BBRC 310, 433 (2003)

Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.