B7-H4 Antibody (935317) [Alexa Fluor® 700]

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Product Details

Summary
Reactivity HuSpecies Glossary
Applications Flow
Clone
935317
Clonality
Monoclonal
Host
Mouse
Conjugate
Alexa Fluor 700

B7-H4 Antibody (935317) [Alexa Fluor® 700] Summary

Immunogen
NS0 mouse myeloma cell line transfected with human B7-H4
Phe29-Ser258
Accession # Q727D3
Specificity
Stains human B7-H4 transfectants but not irrelevant transfectants in flow cytometry.
Isotype
IgG2b
Clonality
Monoclonal
Host
Mouse
Innovator's Reward
Test in a species/application not listed above to receive a full credit towards a future purchase.

Applications/Dilutions

Dilutions
  • Flow Cytometry 0.25-1 ug/10^6 cells

Packaging, Storage & Formulations

Storage
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
Buffer
Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for B7-H4 Antibody (935317) [Alexa Fluor® 700]

  • B7h.5
  • B7H4
  • B7-H4
  • B7H4T-cell costimulatory molecule B7x
  • B7S1
  • B7S1VCTN1
  • B7x
  • B7XPRO1291
  • FLJ22418
  • Immune costimulatory protein B7-H4
  • Protein B7S1
  • T cell costimulatory molecule B7x
  • V-set domain containing T cell activation inhibitor 1
  • V-set domain-containing T-cell activation inhibitor 1
  • Vtcn1

Background

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).
  1. Yi, K.H. and L. Chen (2009) Immunol. Rev. 229:145.
  2. Salceda, S. et al. (2005) Exp. Cell Res. 306:128.
  3. Zang, X. et al. (2003) Proc. Natl. Acad. Sci. 100:10388.
  4. Prasad, V.R. et al. (2003) Immunity 18:863.
  5. Sica, G.L. et al. (2003) Immunity 18:849.
  6. Kryczek, I. et al. (2006) J. Exp. Med. 203:871.
  7. Tringler, B. et al. (2005) Clin. Cancer Res. 11:1842.
  8. Xue, Q. et al. (2010) Stem Cells Dev. 19:27.
  9. Song, H. et al. (2008) Cancer Lett. 266:227.
  10. Park, G.B. et al. (2009) Immunology 128:360.
  11. Zang, X. et al. (2007) Proc. Natl. Acad. Sci. 104:19458.
  12. Krambeck, A.E. et al. (2006) Proc. Natl. Acad. Sci. 103:10391.
  13. Simon, I. et al. (2006) Cancer Res. 66:1570.
  14. Thompson, R.H. et al. (2008) Cancer Res. 68:6054.
  15. Azuma, T. et al. (2009) PloS Med. 6:e1000166.
  16. Suh, W.-K. et al. (2006) Mol. Cell. Biol. 26:6403.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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