Human B7-H4 Antibody Summary
Phe29-Ser258
Accession # Q727D3
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
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Detection of B7‑H4 in HEK293 Human Cell Line Transfected with Human B7-H4 and eGFP by Flow Cytometry. HEK293 human embryonic kidney cell line transfected with either (A) human B7-H4 or (B) irrelevant transfectants and eGFP were stained with Mouse Anti-Human B7-H4 Monoclonal Antibody (Catalog # MAB6576) followed by Allophycocyanin-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # F0101B).
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: B7-H4
B7-H4, also known as VTCN1, B7x and B7S1, is a 50‑80 kDa glycosylated member of the BTN/MOG family of immunomodulatory protein (1, 2). Mature human B7-H4 consists of a 235 amino acid (aa) extracellular domain (ECD) with one Ig-like V-set domain and one Ig-like C2-set domain, a 21 aa transmembrane segment, and a 2 aa cytoplasmic tail (3-5). Within the ECD, human B7-H4 shares 90% aa sequence identity with mouse and rat B7-H4. It shares 22%-28% aa sequence identity with human B7-1, B7-2, B7-H1, B7-H2, B7-H3, and PD‑L2. Alternate splicing of human B7-H4 generates an additional isoform that lacks the first Ig-like domain. B7-H4 is expressed on the surface of activated lymphocytes, macrophages, monocytes, dendritic cells, epithelial cells, and bone marrow-derived mesenchymal stem cells
(4-8). Following binding to activated T cells, B7-H4 serves as a co‑inhibitor of the T cell response. This is accomplished by reverse signaling that can induce either cell cycle arrest, or apoptosis in B7-H4 expressing cells (3-5, 9, 10). B7‑H4 is up‑regulated in several carcinomas in correlation with tumor progression and metastasis (2, 7, 11, 12). A soluble form of B7-H4 is elevated in the serum of ovarian cancer, renal cell carcinoma, and rheumatoid arthritis patients, also in correlation with advanced disease status (13-15). Soluble B7‑H4 functions as a decoy molecule that blocks the inhibitory influence of B7‑H4 on immune activation (15). Despite evidence for the involvement of B7-H4 in immune regulation, mice deficient in its expression do not show significant immune deficiencies, suggesting compensation by other molecules in vivo (16).
- Yi, K.H. and L. Chen (2009) Immunol. Rev. 229:145.
- Salceda, S. et al. (2005) Exp. Cell Res. 306:128.
- Zang, X. et al. (2003) Proc. Natl. Acad. Sci. 100:10388.
- Prasad, V.R. et al. (2003) Immunity 18:863.
- Sica, G.L. et al. (2003) Immunity 18:849.
- Kryczek, I. et al. (2006) J. Exp. Med. 203:871.
- Tringler, B. et al. (2005) Clin. Cancer Res. 11:1842.
- Xue, Q. et al. (2010) Stem Cells Dev. 19:27.
- Song, H. et al. (2008) Cancer Lett. 266:227.
- Park, G.B. et al. (2009) Immunology 128:360.
- Zang, X. et al. (2007) Proc. Natl. Acad. Sci. 104:19458.
- Krambeck, A.E. et al. (2006) Proc. Natl. Acad. Sci. 103:10391.
- Simon, I. et al. (2006) Cancer Res. 66:1570.
- Thompson, R.H. et al. (2008) Cancer Res. 68:6054.
- Azuma, T. et al. (2009) PloS Med. 6:e1000166.
- Suh, W.-K. et al. (2006) Mol. Cell. Biol. 26:6403.
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Cells were transfected with hB7-H4 or a negative control. Cells were stained with MAB6576 using a 1/500 dilution and binding was detected with an anti-mouse 594 secondary antibody.
