Recombinant Mouse B7-H4 His-tag Protein, CF

• Reactivity: Mu
• Applications: Bioactivity
• Format: Carrier-Free

Recombinant Mouse B7-H4 His-tag Protein, CF Summary

• Details of Functionality: Measured by its ability to inhibit anti-CD3 antibody induced IL-2 secretion in human T lymphocytes. The presence of Recombinant Mouse B7-H4 at 10 µg/mL inhibited the anti-CD3 response by >30%.
  Optimal dilutions should be determined by each laboratory for each application.
• Source: Mouse myeloma cell line, NS0-derived mouse B7-H4 protein
  Phe29-Pro258, with a C-terminal 10-His tag
• Accession #: Q7TSP5
• N-terminal Sequence: Phe29
• Protein/Peptide Type: Recombinant Proteins
• Gene: Vtcn1
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Endotoxin Note: <0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

• Theoretical MW: 26.6 kDa.
  Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
• SDS-PAGE: 45-55 kDa, reducing conditions

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS.
• Purity: >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
• Reconstitution Instructions: Reconstitute at 100 μg/mL in sterile PBS.

Notes

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

Alternate Names for Recombinant Mouse B7-H4 His-tag Protein, CF

• 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 B7x and B7S1, is a 50‑80 kDa glycosylated member of the B7 family of immune co‑stimulatory proteins (1, 2). Mature mouse B7-H4 consists of a 230 amino acid (aa) extracellular domain (ECD) with one Ig-like V-set domain and one Ig‑like C2‑set domain which is followed by a hydrophobic C‑terminal region (3‑5). Within the ECD, mouse B7‑H4 shares 90% and 99% aa sequence identity with human and rat B7‑H4, respectively. It shares 21%‑29% aa sequence identity with mouse B7‑1, B7‑2, B7‑H1, B7‑H2, B7‑H3, and PD‑L2. 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). Its binding to activated T cells dampens T cell responses and induces cell cycle arrest in the T cell (3‑5). Reverse signaling can induce either cell cycle arrest or apoptosis in the B7‑H4 expressing cell (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.

Publications for B7-H4 (2154-B7)(2)

Publications using 2154-B7

• Radichev I, Maneva-Radicheva L, Amatya C, Parker C, Ellefson J, Wasserfall C, Atkinson M, Burn P, Savinov A Nardilysin-dependent proteolysis of cell-associated VTCN1 (B7-H4) marks type 1 diabetes development. Diabetes, 2014;63(10):3470-82. 2014 [PMID: 24848066] (ELISA (Standard), N/A)
• Chen X, Quinn EM, Ni H, Wang J, Blankson S, Redmond HP, Wang JH, Feng X B7-H3 participates in the development of experimental pneumococcal meningitis by augmentation of the inflammatory response via a TLR2-dependent mechanism. J. Immunol., 2012;189(1):347-55. 2012 [PMID: 22661093] (In Vivo, Mouse)

Bioinformatics

• Gene Symbol: Vtcn1
• Uniprot:
  • Q7TSP5()