CTLA-4 (E2V1Z) Rabbit mAb (BSA and Azide Free) #26893
- WB
- IHC
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 25-30 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
CTLA-4 (E2V1Z) Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total CTLA-4 protein. Non-specific staining was observed in mouse and human normal and neoplastic liver, in human normal kidney, and in 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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