Recombinant Mouse LILRB4/CD85k/ILT3

英文名 ：Recombinant Mouse LILRB4/CD85k/ILT3

规格 ：10ug/50ug/500ug/1mg

Recombinant Mouse LILRB4/CD85k/ILT3 (CS97)

 

产品说明(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 6His 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

 

制剂（Formulation）

Lyophilized from a 0.2 μm filtered solution of PBS, pH7.4.

 

质量控制（Quality Control） 

Purity:            Greater than 95% as determined by reducing SDS-PAGE.    

Endotoxin:    Less than 0.1 ng/ug (1 EU/ug) 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