Recombinant Rat B7-H4 Fc Chimera (Catalog # 10085-B7) inhibits anti-CD3 antibody induced IFN-gamma secretion by human T cells. The ED50 for this effect is 1-6 μg/mL.
2 μg/lane of Recombinant Rat B7‑H4 Fc Chimera (Catalog # 10085-B7) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at ...read more
>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
Dilutions
Bioactivity
Theoretical MW
52 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
74-85 kDa, reducing conditions
Publications
Read Publication using 10085-B7 in the following applications:
B7-H4,
also known as B7x, B7S1, and V-set
domain-containing T-cell activation inhibitor 1, is a 50-80 kDa glycosylated
member of the B7 family of immunomodulatory proteins (1-5). Mature rat B7-H4 consists of a 235 amino acid (aa) extracellular
domain (ECD) with two Ig-like domains. Within
the ECD, rat B7-H4 shares 90% and 99% aa sequence identity with human and mouse
B7-H4, respectively. 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). 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).
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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