GITRL, Soluble (human) (rec.)
|Synonyms||Glucocorticoid-induced TNF Receptor Ligand; AITRL; Activation-inducible TNF-related Ligand; TNFSF18|
|Source/Host||HEK 293 cells|
|Sequence||The extracellular domain of human GITRL (aa 74-199) is fused at the N-terminus to a FLAG®-tag.|
|Endotoxin Content||<0.06EU/μg purified protein (LAL test; Lonza).|
Reconstitute with sterile water to a concentration of 1mg/ml.
Add 1x PBS to the desired protein concentration.
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Other Product Data||
NCBI link AAH69319.1: GITRL (human)
FLAG is a registered trademark of Sigma-Aldrich Co.
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
Avoid freeze/thaw cycles.
Centrifuge lyophilized vial before opening and reconstitution.
Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
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.