Description
Product Usage Information
Western Blotting: 1:1000
IHC Leica Bond: 1:200 - 1:800
Immunohistochemistry (Paraffin): 1:100 - 1:400
Immunofluorescence (Frozen): 1:50 - 1:200
Flow Cytometry (Fixed/Permeabilized): 1:50 - 1:100
Flow Cytometry (Live): 1:50 - 1:100
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. For a carrier free (BSA and azide free) version of this product see product # 34457 .
Protocol
Available protocols: Western Blotting, IHC Leica Bond, Immunohistochemistry (Paraffin), Immunofluorescence (Frozen), Flow Cytometry (Fixed/Permeabilized), Flow Cytometry (Live)
Specificity / Sensitivity
GITR (E9O9H) Rabbit Monoclonal Antibody recognizes endogenous levels of total mouse GITR protein. Non-specific staining was observed in mouse testis by immunohistochemistry.
Species Reactivity: Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val95 of mouse GITR protein.
Background
TNFRSF18, also known as glucocorticoid-induced tumor necrosis factor-receptor (TNFR)-related protein (GITR) and activation-inducible TNFR family receptor, encodes a type 1 membrane protein of the TNF-receptor superfamily (1). Three alternatively spliced transcript variants encoding distinct isoforms have been reported (2). GITR is an immune cell co-stimulatory receptor expressed constitutively at high levels on CD4 CD25 T regulatory cells (Tregs), at low levels on naïve and memory T cells, and is induced upon T cell activation (3-5). Studies show GITR can also be induced on NK cells, macrophages, and DCs (3,4,6). Although GITR does not have intrinsic enzymatic activity, TNFSF18 (also known as GITRL) expressed on antigen presenting cells binds to GITR, resulting in recruitment of TNFR-associated factor family members and activation of the NF-κB pathway in T cells (7). GITR ligation has been shown to play a role in CD8 T cell activation, cytotoxicity, and memory T cell survival (8-10). In the thymus, GITR is thought to play a key role in dominant immunological self-tolerance through thymic Treg differentiation and expansion (11). Of note, GITR ligation inhibits Treg suppressive function (12-13) and promotes effector T cell resistance to Treg suppression (14-15). Due to the combined effects on both Treg suppression and effector cell activation, GITR represents a unique opportunity for immunotherapeutic intervention in cancer (16).
Alternate Names
AITR; CD357; Gitr; glucocorticoid-induced TNFR-related protein; Tnfrsf18; TNR18; Tumor necrosis factor receptor superfamily member 18; tumor necrosis factor receptor superfamily, member 18
