Recombinant Human VSIG4 His-tag Protein, CF Summary
Product Specifications
Arg20-Pro283, with a C-terminal 6-His tag
Analysis
Product Datasheets
Carrier Free
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
9678-VS
Formulation | Lyophilized from a 0.2 μm filtered solution in PBS. |
Reconstitution | Reconstitute at 200 μg/mL in PBS. |
Shipping | The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. |
Stability & Storage: | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Scientific Data
Recombinant Human VSIG4 His-tag (Catalog # 9678-VS) inhibits IFN-gamma secretion by human peripheral blood mononuclear cells in the presence of anti-CD3 antibody. The ED50 for this effect is 0.5-3 μg/mL.
Reconstitution Calculator
Background: VSIG4
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). The human VSIG4 cDNA encodes 399 amino acids (aa) including a 19 aa signal sequence, a 264 aa extracellular domain (ECD) containing a V-type and a C2-type Ig domain, a 21 aa transmembrane domain and a 95 aa cytoplasmic domain (3). The human VSIG4 ECD shares 84% aa identity with canine VSIG4. Within the IgV domain, it shares 90%, 80% and 78% aa identity with bovine, mouse and rat VSIG4, respectively; these animals lack the C2-type domain. Splice isoforms of 321, 305, 272, 201 and 199 aa lack all or part of the cytoplasmic domain, the C2-type Ig domain and/or the transmembrane domain (5). 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 VSIG4 may be a valuable biomarker in infection and immunity, inflammatory conditions and cancer prognosis (12, 13, 14).
- He, J.Q. et al. (2008) Mol. Immunol. 4041.
- Vogt, L. et al. (2006) J. Clin. Invest. 116:2817.
- Langnaese, K. et al. (2000) Biochim. Biophys. Acta 1492:522.
- Helmy, K. et al. (2006) Cell 124:915.
- Entrez protein Accession # EAX05393, NP_001093901, CAI42052, CAI4205, EAX05394.
- Tanaka, M. et al. (2008) Clin. Exp. Immunol. 154:38.
- Lee, M.Y. et al. (2006) J. Leukoc. Biol. 80:922.
- Gorgani, N.N. et al. (2008) J. Immunol. 181:7902.
- Walker, M.G. (2002) Biochim. Biophys. Acta 1574:387.
- Wiesmann, C. et al. (2006) Nature 444:217.
- Katschke, K.J. et al. (2007) J. Exp. Med. 204:1319.
- Small, A.G. et al. (2016) Swiss Med Wkly. 5:146.
- Roh J. et al. (2017) Oncotarget. 8:58122.
- Kim K.H. et al. (2016) Autophagy. 12:1647.
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