GITR (D9I9D) Rabbit mAb (BSA and Azide Free) #77770
- WB
- IHC
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 25 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This product is the carrier-free version of product #68014. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN, or CUT&Tag assays. If you require a carrier-free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
For standard formulation of this product see product #68014.
Storage
Specificity / Sensitivity
GITR (D9I9D) Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total GITR protein.
Species Reactivity:
Human
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val142 of human 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).
- Nocentini, G. et al. (1997) Proc Natl Acad Sci U S A 94, 6216-21.
- Nocentini, G. et al. (2000) Cell Death Differ 7, 408-10.
- Shimizu, J. et al. (2002) Nat Immunol 3, 135-42.
- Nocentini, G. and Riccardi, C. (2009) Adv Exp Med Biol 647, 156-73.
- McHugh, R.S. et al. (2002) Immunity 16, 311-23.
- Hanabuchi, S. et al. (2006) Blood 107, 3617-23.
- Snell, L.M. et al. (2011) Immunol Rev 244, 197-217.
- Ronchetti, S. et al. (2007) J Immunol 179, 5916-26.
- Kim, I.K. et al. (2015) Nat Med 21, 1010-7.
- Snell, L.M. et al. (2012) J Immunol 188, 5915-23.
- Petrillo, M.G. et al. (2015) Autoimmun Rev 14, 117-26.
- Kanamaru, F. et al. (2004) J Immunol 172, 7306-14.
- Valzasina, B. et al. (2005) Blood 105, 2845-51.
- Stephens, G.L. et al. (2004) J Immunol 173, 5008-20.
- Nishikawa, H. et al. (2008) Cancer Res 68, 5948-54.
- Knee, D.A. et al. (2016) Eur J Cancer 67, 1-10.
Limited Uses
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