CTLA-4 (E2V1Z) & CO-0078-488 SignalStar™ Oligo-Antibody Pair #85716
- IHC
Order Information # 85716
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
Product Description
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
CTLA-4 (E2V1Z) Rabbit mAb (SignalStar™ Conjugate 0078) recognizes endogenous levels of total CTLA-4 protein. Non-specific staining was observed in mouse and human normal and neoplastic liver, human normal kidney, and mouse stomach crypts.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln216 of human CTLA-4 protein.
Background
Cytotoxic T-lymphocyte protein 4 (CTLA-4, CD152) is an Ig superfamily member that negatively regulates early T cell activation (1-4). The CTLA-4 protein is primarily expressed on T cells, including CD8+ cytotoxic T cells, CD4+ helper T cells, and CD4+/FoxP3+ regulatory T cells (1,2). CTLA-4 protein competes with CD28 for B7.1 (CD80) and B7.2 (CD86) binding at the cell surface, which results in the downregulation of T cell activity (5). The activation of SHP-2 and PP2A downstream of CTLA-4 attenuates TCR signaling (6). Research studies indicate that CTLA4 knockout mice display lymphoproliferative disorders leading to early death, confirming the role of CTLA-4 as a negative regulator of T cells (7). Mutations in the corresponding CTLA4 gene are associated with multiple disorders, including insulin-dependent diabetes mellitus, Graves' disease, Hashimoto thyroiditis, celiac disease, systemic lupus erythematosus, and type V autoimmune lymphoproliferative syndrome (8,9). Additional studies demonstrate that CTLA-4 blockade is an effective strategy for tumor immunotherapy (10-12).
- Brunet, J.F. et al. (1987) Nature 328, 267-70.
- Brunet, J.F. et al. (1988) Immunol Rev 103, 21-36.
- Dariavach, P. et al. (1988) Eur J Immunol 18, 1901-5.
- Linsley, P.S. (1995) J Exp Med 182, 289-92.
- Collins, A.V. et al. (2002) Immunity 17, 201-10.
- Rudd, C.E. et al. (2009) Immunol Rev 229, 12-26.
- Waterhouse, P. et al. (1995) Science 270, 985-8.
- Romo-Tena, J. et al. (2013) Autoimmun Rev 12, 1171-6.
- Wang, J. et al. (2014) PLoS One 9, e85982.
- Egen, J.G. et al. (2002) Nat Immunol 3, 611-8.
- Hodi, F.S. et al. (2003) Proc Natl Acad Sci U S A 100, 4712-7.
- Pardoll, D.M. (2012) Nat Rev Cancer 12, 252-64.
Limited Uses
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