TNFRSF18
(Tumor Necrosis Factor Receptor Superfamily, Member 18 (TNFRSF18))
Protein-Typ
Recombinant
Biologische Aktivität
Active
Proteineigenschaft
AA 26-161
Spezies
Human
Quelle
HEK-293 Cells
Aufreinigungstag / Konjugat
Dieses TNFRSF18 Protein ist gelabelt mit His tag.
Sequenz
AA 26-161
Produktmerkmale
This protein carries a polyhistidine tag at the C-terminus. The protein has a calculated MW of 15.4 kDa. The protein migrates as 22-25 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
TNFRSF18
Spezies: Human
Wirt: HEK-293 Cells
Recombinant
The purity of the protein is greater than 95 % as determined by SDS-PAGE and Coomassie blue staining.
FACS
TNFRSF18
Spezies: Human
Wirt: HEK-293 Cells
Recombinant
The purity of the protein is greater than 95 % as determined by SDS-PAGE and Coomassie blue staining.
TNFRSF18
Spezies: Human
Wirt: Wheat germ
Recombinant
WB, ELISA, AP, AA
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Lyophilized
Buffer
PBS, pH 7.4
Handhabung
Please avoid repeated freeze-thaw cycles.
Lagerung
-20 °C
Informationen zur Lagerung
No activity loss was observed after storage at: In lyophilized state for 1 year (4 °C), After reconstitution under sterile conditions for 3 months (-70 °C).
Target
TNFRSF18
(Tumor Necrosis Factor Receptor Superfamily, Member 18 (TNFRSF18))
GITR Protein, TNFRSF18 Protein, AITR Protein, Gitr Protein, CD357 Protein, GITR-D Protein, TNF receptor superfamily member 18 Protein, tumor necrosis factor receptor superfamily, member 18 Protein, TNFRSF18 Protein, Tnfrsf18 Protein
Hintergrund
Glucocorticoid-induced TNFR-related protein (GITR) is also known as Tumor necrosis factor receptor superfamily member 18 (TNFRSF18), activation-inducible TNFR family receptor (AITR), CD antigen CD357, which is a member of the tumor necrosis factor receptor (TNF-R) superfamily. GITR is receptor for TNFSF18, which seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. GITR also mediated NF-kappa-B activation via the TRAF2/NIK pathway.