Recombinant Human HLA-G protein

>90% as determined by SDS-PAGE

Please contact with the lab for this information.

A DNA sequence encoding the human HLA-G (Met29-His117) was fused with GST tag

P17693

E.coli

Homo sapiens (Human)

36.32 kDa

Supplied as solution form in PBS pH 7.5 or lyophilized from PBS pH 7.5.

In general, proteins are provided as lyophilized powder/frozen liquid. They are shipped out with dry ice/blue ice unless customers require otherwise.

Use a manual defrost freezer and avoid repeated freeze thaw cycles.
Store at 2 to 8 °C for one week .
Store at -20 to -80 °C for twelve months from the date of receipt.

Reconstitute in sterile water for a stock solution.A copy of datasheet will be provided with the products, please refer to it for details.

Isoform 1:
Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface . In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins . Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance . Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy. Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling . Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance. May play a role in balancing tolerance and antiviral-immunity at maternal-fetal interface by keeping in check the effector functions of NK, CD8+ T cells and B cells . Reprograms B cells toward an immune suppressive phenotype via LILRB1 . May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes . Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites

HLA class I histocompatibility antigen, alpha chain G,HLA G antigen,MHC class I antigen G,

For research use only .