GITRL Mouse anti-Human, Clone: 109114, Invitrogen
Mouse Monoclonal Antibody
Manufacturer: Invitrogen MA523852
In sandwich ELISAs, no cross-reactivity or interference with recombit human (rh) APRIL, rhLIGHT, rhTNF-alpha, or rhVEGI is observed. Reconstitute at 0.5 mg/mL in sterile PBS. Endoxin level is <0.10 EU per 1 µg of the antibody by the LAL method.The tumor necrosis factor (TNF) and TNF receptor (TNFR) gene superfamilies regulate numerous biological functions including cell proliferation, differentiation, and survival through regulating the activation of the transcription factor NF-kappa-B and various mitogen-activated protein kinases. The glucocorticoid-induced tumor necrosis factor receptor (GITR) is an emerging member of this family that is expressed on CD4+ CD25+ regulatory T cells and appears to have crucial immune regulation functions. Its ligand GITRL is expressed in endothelial and antigen-presenting cells and can activate NF-kappa-B, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR. Domit negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-kappa-B activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.
|PBS with 5% trehalose and No Preservative|
|RP1-15D23.1, AITRL, GITRL, TL6, hGITRL, AITR ligand, GITR ligand, activation-inducible TNF-related ligand, glucocorticoid-induced TNF-related ligand, glucocorticoid-induced TNFR-related protein ligand, tumor necrosis factor ligand superfamily member 18|
|-20° C, Avoid Freeze/Thaw Cycles|
|ELISA, Flow Cytometry, Neutralization|
|Sf 21-derived recombit human GITR Ligand/TNFSF18Glu52-Ser177|
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