Recombinant Mouse LILRB4/CD85k/ILT3 Protein, CF Summary
Product Specifications
Gly24-Lys238, 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.
9095-T4
| Formulation | Lyophilized from a 0.2 μm filtered solution in PBS. |
| Reconstitution | Reconstitute at 500 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
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When Recombinant Mouse LILRB4/CD85k/ ILT3 is coated onto a microplate at 2 µg/mL, Recombinant Human Angiopoietin-like Protein 7 (Catalog # 914-AN) binds with a typical ED50 of 20-120 ng/mL.
Reconstitution Calculator
Background: LILRB4/CD85k/ILT3
LILRB4, also known as ILT3, CD85k, and LIR-5, is an approximately 60 kDa transmembrane glycoprotein that negatively regulates immune cell activation (1). Mature mouse LILRB4 consists of a 215 amino acid (aa) extracellular domain with two Ig-like domains, a 22 aa transmembrane segment, and a 75 aa cytoplasmic domain with 3 immunoreceptor tyrosine-based inhibitory motifs (ITIM) (2). Within the ECD, mouse LILRB4 shares 45% and 77% aa sequence identity with human and rat LILRB4, respectively. Alternative splicing of mouse LILRB4 generates a potentially soluble isoform that lacks the transmembrane segment (2). LILRB4 is expressed on dendritic cells (DC), monocytes, macrophages, and vascular endothelial cells (EC) (3, 6, 7). Ligation of LILRB4 triggers ITIM-mediated inhibition of cell-activating signaling, leading to enhanced immune tolerance and reduced allogeneic graft rejection (3, 5, 8, 9). Soluble LILRB4 induces the differentiation of CD8+ T suppressor cells (Ts) that can inhibit the effector functions of CD4+ Th cells and CD8+ CTL (5, 8, 10). In turn, CD8+ Ts cells induce LILRB4 up-regulation and a tolerogenic phenotype in monocytes, DC, and EC (6, 7, 9, 11, 12).
- Vlad, G. et al. (2010) Int. Rev. Immunol. 29:119.
- Castells, M.C. et al. (1994) J. Biol. Chem. 269:8393.
- Cella, M. et al. (1997) J. Exp. Med. 185:1743.
- Heinzmann, A. et al. (2000) Eur. J. Immunogenet. 27:121.
- Suciu-Foca, N. et al. (2007) J. Immunol. 178:7432.
- Gleissner, C.A. et al. (2007) Eur. J. Immunol. 37:177.
- Manavalan, J.S. et al. (2004) Int. Immunol. 16:1055.
- Vlad, G. and N. Suciu-Foca (2012) Exp. Mol. Pathol. 93:294.
- Chang, C.C. et al. (2002) Nat. Immunol. 3:237.
- Vlad, G. et al. (2006) Int. Immunopharmacol. 6:1889.
- Manavalan, J.S. et al. (2003) Transpl. Immunol. 11:245.
- Brenk, M. et al. (2009) J. Immunol. 183:145.
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