TNFSF18 Protein (AA 74-199) (His tag)
-
- Target See all TNFSF18 Proteins
- TNFSF18 (Tumor Necrosis Factor (Ligand) Superfamily, Member 18 (TNFSF18))
- Protein Type
- Recombinant
- Protein Characteristics
- AA 74-199
-
Origin
- Human
-
Source
- HEK-293 Cells
- Purification tag / Conjugate
- This TNFSF18 protein is labelled with His tag.
- Purpose
- GITRL, Soluble (human) (rec.) (His)
- Specificity
- The extracellular domain of human GITRL (aa 74-199) is fused at the C-terminus to a His-tag.
- Cross-Reactivity
- Human
- Characteristics
- The extracellular domain of human GITRL (aa 74-199) is fused at the C-terminus to a His-tag.
- Purity
- >90 % (SDS-PAGE)
- Sterility
- Sterile filtered
- Endotoxin Level
- <0.06EU/μg purified protein (LAL test).
- Top Product
- Discover our top product TNFSF18 Protein
-
-
- Restrictions
- For Research Use only
-
- Format
- Lyophilized
- Concentration
- Lot specific
- Buffer
- Lyophilized from 0.2μm-filtered solution in PBS.
- Handling Advice
- After reconstitution, prepare aliquots and store at -20 °C. Avoid freeze/thaw cycles. Centrifuge lyophilized vial before opening and reconstitution. PBS containing at least 0.1 % BSA should be used for further dilutions.
- Storage
- 4 °C,-20 °C
- Storage Comment
-
Short Term Storage: +4°C
Long Term Storage: -20°C
Use & Stability: Stable for at least 6 months after receipt when stored at -20°C. Working aliquots are stable for up to 3 months when stored at -20°C.
- Expiry Date
- 6 months
-
- Target
- TNFSF18 (Tumor Necrosis Factor (Ligand) Superfamily, Member 18 (TNFSF18))
- Alternative Name
- GITRL (TNFSF18 Products)
- Background
-
Glucocorticoid-induced TNF Receptor Ligand, AITRL, Activation-inducible TNF-related Ligand, TNFSF18
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.
- Molecular Weight
- ~17kDa (SDS-PAGE)
-