B7-H4 (D1M8I) XP® Rabbit mAb (BSA and Azide Free) #17188
- WB
- IHC
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 75 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This product is the carrier free version of product #14572. 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. 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
B7-H4 (D1M8I) XP® Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total B7-H4 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala141 of human B7-H4 protein.
Background
B7 homolog 4 (B7-H4, VTCN1) is a member of the B7 family of cell surface ligands that regulate T cell activation and immune responses (1-3). B7-H4 protein contains two extracellular Ig-like V-type domains, a transmembrane domain, and a short, two amino acid intracellular domain (3). The B7-H4 protein is shown to inhibit T cell activation, proliferation, and cytokine production (1,4,5). Although B7-H4 mRNA is widely expressed, B7-H4 protein is restricted to antigen presenting cells and B cells (1). The B7-H4 protein is also found in several tumor types, including ovarian cancer and breast cancer (6). Research studies indicate that B7-H4 protein is present on the surface of ovarian tumor cells, and that targeted inhibition of B7-H4 using recombinant antibodies restores T cell activation pathways. These studies suggest some potential therapeutic value in blocking B7-H4 function and restoring T cell function in cancer patients (7,8).
- Sica, G.L. et al. (2003) Immunity 18, 849-61.
- Prasad, D.V. et al. (2003) Immunity 18, 863-73.
- Zang, X. et al. (2003) Proc Natl Acad Sci U S A 100, 10388-92.
- He, C. et al. (2011) Clin Dev Immunol 2011, 695834.
- Yi, K.H. and Chen, L. (2009) Immunol Rev 229, 145-51.
- Salceda, S. et al. (2005) Exp Cell Res 306, 128-41.
- Dangaj, D. and Scholler, N. (2013) Oncoimmunology 2, e25913.
- Dangaj, D. et al. (2013) Cancer Res 73, 4820-9.
Limited Uses
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