TNFSF18 Protein (AA 45-173, Extracellular Domain, Soluble) (DYKDDDDK Tag)
Quick Overview for TNFSF18 Protein (AA 45-173, Extracellular Domain, Soluble) (DYKDDDDK Tag) (ABIN1344404)
Target
See all TNFSF18 ProteinsProtein Type
Biological Activity
Origin
Source
Application
Purity
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Protein Characteristics
- Soluble, Extracellular Domain, AA 45-173
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Purification tag / Conjugate
- This TNFSF18 protein is labelled with DYKDDDDK Tag.
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Purpose
- GITRL, Soluble (mouse) (rec.)
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Specificity
- Binds to mouse GITR.
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Cross-Reactivity
- Mouse
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Characteristics
- The extracellular domain of mouse GITRL (aa 45-173) is fused at the N-terminus to a FLAG®-tag.
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Sterility
- Sterile filtered
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Endotoxin Level
- <0.1EU/μg purified protein (LAL test).
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Biological Activity Comment
- Induces GITR-mediated NF-kappaB activation in HEK 293 cells.
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Application Notes
- Optimal working dilution should be determined by the investigator.
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Restrictions
- For Research Use only
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Format
- Liquid
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Concentration
- 0.5 mg/mL
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Buffer
- 0.2μm-filtered solution in 10 mM glycine, pH 10.0.
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Handling Advice
- After opening, prepare aliquots and store at -20 °C. Avoid freeze/thaw cycles. For maximum product recovery after thawing, centrifuge the vial before opening the cap.
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Storage
- 4 °C,-20 °C
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Storage Comment
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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.
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Expiry Date
- 6 months
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- TNFSF18 (Tumor Necrosis Factor (Ligand) Superfamily, Member 18 (TNFSF18))
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Alternative Name
- GITRL
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Background
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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.
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Molecular Weight
- ~22kDa (SDS-PAGE)
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UniProt
- Q7TS55
Target
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