GITRL polyclonal, anti-human, mouse

Protein Family: Enzymes

Pathway and Disease: Signaling Molecules and Interaction

Description:
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-kappaB 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-kappaB, 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-kappaB activation, suggesting that the GITRL-GITR pathway involves both NIK and TRAF2.

Alternate Names: GITRL, AITRL

Application Notes: E: 1:500-1:1,000; WB: 1:100-1:500; ICC: 1:100-1:500

Accession No.: Q9UNG2

Antigen: KLH-conjugated synthetic peptide encompassing a sequence within human GITRL.

Format: Each vial contains 0.1 ml IgG in PBS pH 7.4 with 0.02% sodium azide. Antibody was purified by immunogen affinity chromatography.

Storage:
Store at -20°C. Minimize freeze-thaw cycles. Product is guaranteed one year from the date of shipment.