Invitrogen™ GITRL Polyclonal Antibody

Descrizione

Suggested positive controls are human pancrease and mouse spleen tissue lysates.

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.