CTLA-4 (E2V1Z) Rabbit mAb (BSA and Azide Free) #55226
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Product Name
- 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. 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.
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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