Recombinant Human LILRB4 (C-Fc

Recombinant Human LILRB4 (C-Fc) (CW49)

 

产品说明(Description)

Recombinant Human Leukocyte Immunoglobulin-like Receptor Subfamily B Member 4 is produced by our Mammalian expression system and the target gene encoding Gln22-Glu259 is expressed with a Fc tag at the C-terminus.

Accession #: Q8NHJ6

Known as:  Leukocyte immunoglobulin-like receptor subfamily B member 4; Mast cell surface Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.glycoprotein Gp49B; CD85k; Lilrb4; Gp49b

 

制剂（Formulation）

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

 

质量控制（Quality Control） 

Purity:            Greater than 90% as determined by reducing SDS-PAGE.

Endotoxin:    Less than 0.1 ng/μg (1 EU/μg) as determined by LAL test.

 

 

复溶（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 distilled water.
Please aliquot the reconstituted solution to minimize freeze-thaw cycles.

 

保存（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.

 

背景（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.

 

电泳(SDS-PAGE)

 

FOR RESEARCH USE ONLY.