Recombinant Mouse PD-L2 (C-Fc)

Description

EnkiLife provides the Recombinant Mouse PD-L2 (C-Fc) protein,aslo know as Programmed cell death 1 ligand 2;Pdcd1lg2;PD-1 ligand 2;PD-L2,PDCD1 ligand 2,B7-DC,CD273;, which features high purity, high activity, and high stability. It can be applied in scientific research, biopharmaceuticals, and other fields.Purity:Greater than 95% as determined by reducing SDS-PAGE;Endotoxin Level:<1 EU/µg as determined by LAL test.;Construction:Recombinant Mouse Programmed Cell Death 1 Ligand 2 is produced by our Mammalian expression system and the target gene encoding Leu20-Arg219 is expressed with a human IgG1 Fc tag at the C-terminus.Accession:Q9WUL5. Expression Host:Human Cells.Species:Mouse.Predicted Molecular Mass:49.7 KDa. Background:Programmed cell death 1 ligand 2 (PD-L2), also known as butyrophilin B7-DC or PDCD1 ligand 2, belongs to the member of B7 family which can regulate the activation and tolerance of T cells. PD-L2 is one ligand for Programmed cell death 1(PD-1), and the other is PD-L1. These two ligands shares 34% aa sequence identity. Mouse PD-L2 gene encodes a 273 amino acids (aa) protein with a putative 19 aa signal peptide, a 201 aa extracellular region , a 21 aa transmembrane domain and a 32 aa cytoplasmic region. The mouse PD-L2 gene is highly expressed in heart, placenta, pancreas, lung and liver while expressed weakly in spleen, lymph nodes and thymus. Besides, the expression of PD-L2 gene can be induced on dendritic cells grown from peripheral blood mononuclear cells under CSF2 and IL4/interleukin-4 treatment, and up-regulated by IFNG/IFN-gamma stimulation in monocytes. PD-L2 usually functions in a PDCD1-independent manner and is involved in regulating costimulatory signal which is essential for T-cell proliferation and IFNG production. Recent studies demonstrate that the expression of PD-L2 on the tumor cells promotes CD8 T cell–mediated rejection of tumor cells, at both the induction and effector phase of antitumor immunity. Moreover, PD-L2 binds to PD-1 cells and enhances T cell killing in a PD-1–independent mechanism.