Recombinant Mouse VSIG4 His-tag Protein, CF

Recombinant Mouse VSIG4 (Catalog # 9747-VS) inhibits IFN-gamma secretion by human peripheral blood mononuclear cells in the presence ofanti-CD3 antibody. The ED50 for this effect is 0.5-2.5 μg/mL.

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

Recombinant Mouse VSIG4 His-tag Protein, CF Summary

• Details of Functionality: Measured by its ability to inhibit anti-CD3 antibody induced IFN-gamma secretion by human peripheral blood mononuclear cells (PBMC). The ED₅₀ for this effect is 0.5-2.5 μg/mL.
• Source: Mouse myeloma cell line, NS0-derived mouse VSIG4 protein
  His20-Pro187, with a C-terminal 6-His tag
• Accession #: NP_808457
• N-terminal Sequence: His20
• Protein/Peptide Type: Recombinant Proteins
• 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

• Dilutions:
  • Bioactivity
• Theoretical MW: 20 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: 29-38 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 200 μg/mL in PBS.

Notes

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

Alternate Names for Recombinant Mouse VSIG4 His-tag Protein, CF

• CRIg
• Ig superfamily protein
• Protein Z39Ig
• V-set and immunoglobulin domain containing 4
• V-set and immunoglobulin domain-containing protein 4
• VSIG4
• Z39IG
• Z39IGcomplement receptor of the immunoglobulin superfamily

Background

VSIG4 (Vset and immunoglobulin domain containing 4), also known as complement receptor immunoglobulin (CRIg) and Z39IG, is a 45 kDa, type I transmembrane protein of the B7 family within the Ig superfamily that is expressed only in tissue resident macrophages (1-4). The gene is located on the X chromosome (2). Mouse VSIG4 is synthesized as a 280 amino acid (aa) precursor that contains a signal sequence, an IgV-type immunological domain, one potential N-linked glycosylation site, and a single transmembrane domain (4). The IgV domain of mouse VSIG4 shares 86% and 80% aa sequence identity with the IgV domains of rat and human VSIG4, respectively. VSIG4 is specifically expressed on macrophages in the thymic medulla, peritoneum, alveoli, synovia, adipose and heart, liver Kupffer cells, placental Hofbauer cells, and atherosclerotic foam cells (1-4, 6-9). It is absent on infiltrating macrophages (8). VSIG4 is a complement receptor that binds C3b and iC3b fragments, internalizes them to recycling endosomes, and is recycled to the cell surface (4, 6). It contributes significantly to innate immunity by binding and phagocytosis of complement opsonized invading pathogens (4, 8, 10). Binding of either native or recombinant soluble VSIG4 to C3b inhibits complement amplification through the alternative, but not classical, pathway (10, 11). VSIG4 is also a negative regulator of mouse and human T cell activation (2). Although VSIG4 engagement may activate NF kappa B and thus be proinflammatory in some cases, many of its activities are important in resolving, rather than initiating, inflammation (1, 2, 7, 10, 11). There is emerging evidence in human conditions that VSIG-4 may be a valuable biomarker in infection and immunity, inflammatory conditions and cancer prognosis (12-14).

1. He, J.Q. et al. (2008) Mol. Immunol. 45:4041.
2. Vogt, L. et al. (2006) J. Clin. Invest. 116:2817.
3. Langnaese, K. et al. (2000) Biochim. Biophys. Acta 1492:522.
4. Helmy, K.Y. et al. (2006) Cell 124:915.
5. Entrez protein Accession # EAX05393, NP_001093901, CAI42052, CAI4205, EAX05394.
6. Tanaka, M. et al. (2008) Clin. Exp. Immunol. 154:38.
7. Lee, M.Y . et al. (2006) J. Leukoc. Biol. 80:922.
8. Gorgani, N.N. et al. (2008) J. Immunol. 181:7902.
9. Walker, M.G. (2002) Biochim. Biophys. Acta 1574:387.
10. Wiesmann, C. et al. (2006) Nature 444:217.
11. Katschke, K.J. et al. (2007) J. Exp. Med. 204:1319.
12. Small, A.G. et al. (2016) Swiss Med. Wkly. 146:w14301.
13. Roh J., et al. (2017) Oncotarget 8:58122.
14. Kim K.H., et al. (2016) Autophagy 12:1647.

Bioinformatics

• Uniprot:
  • NP_808457()