Human leukocyte antigen G,HLA-G ELISA KIT

SKU: E0443Hu

Size:96 Tests-1 Kit

Background:[Isoform 1]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed:23184984, PubMed:29262349, PubMed:19304799). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PubMed:7584149, PubMed:8805247). 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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799, PubMed:20448110, PubMed:27859042). 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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799). Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling (PubMed:19304799). 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 (PubMed:20448110, PubMed:27859042). 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 (PubMed:10190900, PubMed:11290782, PubMed:24453251). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed:24453251). May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes (PubMed:20179272, PubMed:26460007). Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites (PubMed:16809620). {ECO:0000269|PubMed:10190900, ECO:0000269|PubMed:11290782, ECO:0000269|PubMed:16366734, ECO:0000269|PubMed:16809620, ECO:0000269|PubMed:19304799, ECO:0000269|PubMed:20179272, ECO:0000269|PubMed:20448110, ECO:0000269|PubMed:23184984, ECO:0000269|PubMed:24453251, ECO:0000269|PubMed:26460007, ECO:0000269|PubMed:27859042, ECO:0000269|PubMed:29262349, ECO:0000269|PubMed:7584149, ECO:0000269|PubMed:8805247}.; [Isoform 2]: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782). {ECO:0000269|PubMed:11290782, ECO:0000305}.; [Isoform 3]: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782). {ECO:0000269|PubMed:11290782, ECO:0000305}.; [Isoform 4]: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782). {ECO:0000269|PubMed:11290782, ECO:0000305}.; [Isoform 5]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed:23184984, PubMed:29262349, PubMed:19304799). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PubMed:7584149, PubMed:8805247). 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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799, PubMed:20448110). 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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799). Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling (PubMed:19304799). 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 (PubMed:20448110). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed:24453251). {ECO:0000269|PubMed:16366734, ECO:0000269|PubMed:19304799, ECO:0000269|PubMed:20448110, ECO:0000269|PubMed:23184984, ECO:0000269|PubMed:24453251, ECO:0000269|PubMed:29262349, ECO:0000269|PubMed:7584149, ECO:0000269|PubMed:8805247}.; [Isoform 6]: Likely does not bind B2M and presents peptides. {ECO:0000305}.; [Isoform 7]: Likely does not bind B2M and presents peptides. {ECO:0000305}.

Research_area:

Applications:ELISA

Target_protein:HLA-G

Reactivity:Human

Assay type:Sandwich

Sensitivity:14.54ng/L

Detection range:30-9000ng/L

Sample type:Serum, plasma or other biological fluids

Full product name:leukocyte antigen G

Species:Human

Storage:2-8ºC

Assay time:1h 30m

UniProt accession:P17693

MASS(Da):38224

GeneID:3135

Synonyms:HLA-G HLA-6.0 HLAG

Gene names:HLA-G

Standard solution:9600ng/L