Render Target: STATIC
Render Timestamp: 2024-12-26T11:08:23.301Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-08-30 10:36:13.085
Product last modified at: 2024-12-17T19:01:11.060Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

GITR (D9I9D) Rabbit mAb (BSA and Azide Free) #77770

Filter:
  • 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.

    BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

    Formulation

    Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

    For standard formulation of this product see product #68014.

    Storage

    Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

    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).
    1. Nocentini, G. et al. (1997) Proc Natl Acad Sci U S A 94, 6216-21.
    2. Nocentini, G. et al. (2000) Cell Death Differ 7, 408-10.
    3. Shimizu, J. et al. (2002) Nat Immunol 3, 135-42.
    4. Nocentini, G. and Riccardi, C. (2009) Adv Exp Med Biol 647, 156-73.
    5. McHugh, R.S. et al. (2002) Immunity 16, 311-23.
    6. Hanabuchi, S. et al. (2006) Blood 107, 3617-23.
    7. Snell, L.M. et al. (2011) Immunol Rev 244, 197-217.
    8. Ronchetti, S. et al. (2007) J Immunol 179, 5916-26.
    9. Kim, I.K. et al. (2015) Nat Med 21, 1010-7.
    10. Snell, L.M. et al. (2012) J Immunol 188, 5915-23.
    11. Petrillo, M.G. et al. (2015) Autoimmun Rev 14, 117-26.
    12. Kanamaru, F. et al. (2004) J Immunol 172, 7306-14.
    13. Valzasina, B. et al. (2005) Blood 105, 2845-51.
    14. Stephens, G.L. et al. (2004) J Immunol 173, 5008-20.
    15. Nishikawa, H. et al. (2008) Cancer Res 68, 5948-54.
    16. Knee, D.A. et al. (2016) Eur J Cancer 67, 1-10.
    For Research Use Only. Not For Use In Diagnostic Procedures.
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