Description
Recombinant Mouse LILRB4/CD85k/ILT3 Protein (His Tag) | PKSM041309 | Gentaur US, UK & Europe Disrtribition
Synonyms: Leukocyte immunoglobulin-like receptor subfamily B member 4; Mast cell surface glycoprotein Gp49B; CD85k; Lilrb4; Gp49b
Active Protein: N/A
Activity: Recombinant Mouse LILRB4 is produced by our Mammalian expression system and the target gene encoding Gly24-Lys238 is expressed with a 6His tag at the C-terminus.
Protein Construction: Recombinant Mouse LILRB4 is produced by our Mammalian expression system and the target gene encoding Gly24-Lys238 is expressed with a 6His tag at the C-terminus.
Fusion Tag: C-His
Species: Mouse
Expressed Host: Human Cells
Shipping: This product is provided as lyophilized powder which is shipped with ice packs.
Purity: > 95 % as determined by reducing SDS-PAGE.
Endotoxin: < 1.0 EU per μg as determined by the LAL method.
Stability and Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Molecular Mass: 24.9 kDa
Formulation: Lyophilized from a 0.2 μm filtered solution of PBS, pH7.4.
Reconstitution: Please refer to the printed manual for detailed information.
Background: Mouse Leukocyte Immunoglobulin-like Receptor Subfamily B Member 4 (LILRB4/CD85k/ILT3) is an approximately transmembrane glycoprotein that negatively regulates immune cell activation. 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). 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. LILRB4 is expressed on dendritic cells (DC), monocytes, macrophages, and vascular endothelial cells (EC). Ligation of LILRB4 triggers ITIM-mediated inhibition of cellactivating signaling, leading to enhanced immune tolerance and reduced allogeneic graft rejection. Soluble LILRB4 induces the differentiation of CD8+ T suppressor cells (Ts) that can inhibit the effector functions of CD4+ Th cells and CD8+ CTL. In turn, CD8+ Ts cells induce LILRB4 up-regulation and a tolerogenic phenotype in monocytes, DC, and EC.
Research Area: N/A
