Recombinant Mouse Leukocyte Ig-Like Receptor B4/LILRB4/CD85k/ILT3 (C-Fc)

Cat.No.: CW52

Description
Recombinant Mouse Leukocyte Immunoglobulin-like Receptor Subfamily B Member 4 is produced by our Mammalian expression system and the target gene encoding Gly24-Lys238 is expressed with a Fc tag at the C-terminus.
Accession #:Q64281
Known as:Leukocyte immunoglobulin-like receptor subfamily B member 4; Mast cell surface glycoprotein Gp49B; CD85k; Lilrb4; Gp49b
Formulation
Lyophilized from a 0.2 μm filtered solution of 50 mM Tris-HCl,100mM Glycine,pH7.5.
Quality Control
Purity:Greater than 95% as determined by reducing SDS-PAGE.
Endotoxin:Less than 0.1 ng/?g (1 EU/?g) as determined by LAL test.
Reconstitution
Always centrifuge tubes before opening. Do not mix by vortex or pipetting.
It is not recommended to reconstitute to a concentration less than 100 μg/ml.
Dissolve the lyophilized protein in ddH2O.
Please aliquot the reconstituted solution to
Storage
Lyophilized protein should be stored at < -20°C, though stable at room temperature for 3 weeks.
Reconstituted protein solution can be stored at 4-7°C for 2-7 days.
Aliquots of reconstituted samples are stable at < -20°C for 3 months.
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.

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