GITRL Polyclonal Antibody, Biotin, PeproTech®, Invitrogen™

Description

AA Sequence of recombinant protein: METAKEPCMA KFGPLPSKWQ MASSEPPCVN KVSDWKLEIL QNGLYLIYGQ VAPNANYNDV APFEVRLYKN KDMIQTLTNK SKIQNVGGTY ELHVGDTIDL IFNSEHQVLK NNTYWGIILL ANPQFIS. Preparation: Produced from sera of rabbits immunized with highly pure Recombinant Human AITRL. Anti-Human AITRL-specific antibody was purified by affinity chromatography and then biotinylated. Sandwich ELISA: To detect hAITRL by sandwich ELISA (using 100 μL/well antibody solution) a concentration of 0.25-1.0 μg/mL of this antibody is required. This biotinylated polyclonal antibody, in conjunction with PeproTech Polyclonal Anti-Human AITRL (500-P244) as a capture antibody, allows the detection of at least 0.2-0.4 ng/well of Recombinant hAITRL. Western Blot: To detect hAITRL by Western Blot analysis this antibody can be used at a concentration of 0.1-0.2 μg/mL. Used in conjunction with compatible secondary reagents the detection limit for Recombinant hAITRL is 1.5-3.0 ng/lane, under either reducing or non-reducing conditions. 500-P244BT-1MG will be provided as 2 x 500 μg

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. Dominant 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.