Render Target: SSR
Render Timestamp:
4/1/2025, 11:47:18 AM EDT
4/1/2025, 3:47:18 PM UTC
Commit: 461ca8d8fe5b1efd4c01fc87e5b5eb592e2d154a
XML generation date: 2025-03-25 22:05:24.987
Product last modified at: 2025-03-27T08:00:12.054Z
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PDP - Template Name: Oligo Antibody Pair
PDP - Template ID: *******46423d7

GITR (E9O9H) & CO-0186-594 SignalStar Oligo-Antibody Pair #84016

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  • IHC

Order Information # 84016

This product is not sold separately. Please see the SignalStar™ Multiplex IHC Panel Builder Tool for ordering information.

    Product Information

    Product Usage Information

    Application Dilution
    SignalStar™ Leica Bond 1:50 - 1:200
    SignalStar™ Manual 1:50 - 1:200

    Storage

    SignalStar conjugates are supplied in PBS (pH 7.2), less than 0.1% sodium azide, 2 mM EDTA, 0.05% Triton X-100, 2 mg/mL BSA, and 50% glycerol. Complementary oligos are supplied in nuclease-free water. Store at -20°C. Do not aliquot the antibody. All components in this kit are stable for at least 12 months when stored at the recommended temperature.

    Product Description

    SignalStar multiplex immunohistochemistry (IHC) is an advanced technology for labeling multiple proteins simultaneously in tissue samples using specific primary antibodies and fluorescent detection reagents. This technology offers accuracy and reliability in visualizing and analyzing protein expression while maintaining spatial context and tissue architecture.

    SignalStar Oligo-Antibody Pairs are compatible with the SignalStar Multiplex IHC Buffer Kits for use in fluorescent multiplex imaging experiments. This product includes the oligo-conjugated antibodies and complementary oligos required for labeling your target protein on up to 10 slides. SignalStar Multiplex IHC Buffer Kits are required to amplify and image the target signal. Multiple oligo-antibody pairs can be conveniently combined into a multiplex panel using the SignalStar Multiplex IHC Panel Builder. SignalStar Multiplex IHC Kits & Reagents are not compatible with all of Cell Signaling Technology® products and protocols that are recommended for use in immunohistochemical assays.

    Protocol

    Specificity / Sensitivity

    GITR (E9O9H) Rabbit mAb (SignalStar® Conjugate 0186) 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).
    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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