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

SKU: PKSM041393-50

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

 

SKU # PKSM041393
Expression Host HEK293 Cells

 

 

Description

Synonyms CD85k, Gp49b, Leukocyte immunoglobulin-like receptor subfamily B member 4, Lilrb4, Mast cell surface glycoprotein Gp49B
Species Mouse
Expression Host HEK293 Cells
Sequence Gly24-Lys238
Accession Q64281
Calculated Molecular Weight 51.0 kDa
Observed Molecular Weight 65-85 kDa
Tag C-Fc
Bio-activity Not validated for activity
  

 

Properties

Purity > 95 % as determined by reducing SDS-PAGE.
Endotoxin < 1.0 EU per μg of the protein as determined by the LAL method.
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.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from a 0.2 μm filtered solution of 50 mM Tris-HCl, 100mM Glycine, pH 7.5.
Normally 5% - 8% trehalose, mannitol and 0.01% Tween 80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
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.