Rabbit polyclonal antibody to GITRLThe 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-kappaB and various mitogen-activated protein kinases (reviewed in 1). 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 (2,3). Its ligand GITRL is expressed in endothelial and antigen-presenting cells (4) and can activate NF-kappaB, induce both pro- and anti-apoptotic effects, inhibit the suppressive activity of regulatory T cells, and co-stimulate responder T cells through GITR (5). Dominant negative forms of NIK and TRAF2 expressed in transfected 293 cells substantially inhibited NF-kappaB activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2 (4).
Immunogen
Recombinant human GITR ligand
Key Feature
Clonality
Polyclonal
Host Species
Rabbit
Tested Applications
ELISAICC/IFWB
ICC/IF:1:200~1:500 WB:1:500~1:2000 Notes:Optimal dilutions/concentrations should be determined by the researcher.
Species Reactivity
HumanMouse
Concentration
1mg/ml
Purification
Affinity purified
Target Information
Gene Synonyms
AITRL GITRL
Target
GITRL
Tissue Specificity
This antibody is specific for GITRL
Application
Application
Immunocytochemistry of GITRL in THP-1 cells with GITRL antibody at 10 ug/ml.
Application
Western blot analysis of (A) 5 ng, (B) 25 ng, and (C) 50 ng of purified recombinant GITRL with ITRL antibody at 1 ug/ml.