R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
CTLA-4 (E2V1Z) Rabbit mAb (BSA and Azide Free) #26893
Filter:
- 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 product is the carrier free version of product #53560. 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. Optimal dilutions/concentrations should be determined by the end user.
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
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
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.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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