WB, IHC-Bond, IHC-P
H
Endogenous
25
Rabbit IgG
#Q9Y5U5
8784
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| IHC Leica Bond | 1:400 |
| Immunohistochemistry (Paraffin) | 1:400 |
Storage
For a carrier-free (BSA and azide free) version of this product see product #77770
Specificity / Sensitivity
Species Reactivity:
Human
Species predicted to react based on 100% sequence homology
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.
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.
Species Reactivity
Species reactivity is determined by testing in at least one approved application (e.g., western blot).
Western Blot Buffer
IMPORTANT: For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
Applications Key
WB: Western Blotting IHC-Bond: IHC Leica Bond IHC-P: Immunohistochemistry (Paraffin)
Cross-Reactivity Key
H: human M: mouse R: rat Hm: hamster Mk: monkey Vir: virus Mi: mink C: chicken Dm: D. melanogaster X: Xenopus Z: zebrafish B: bovine Dg: dog Pg: pig Sc: S. cerevisiae Ce: C. elegans Hr: horse GP: Guinea Pig Rab: rabbit All: all species expected
Trademarks and Patents
Limited Uses
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