Mouse Monoclonal HLAG antibody. Suitable for Flow Cyt and reacts with Human samples. Cited in 31 publications. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human HLA-G.
IgG1
Mouse
pH: 7.4
Preservative: 0.097% Sodium azide
Constituents: PBS
Liquid
Monoclonal
Flow Cyt | |
---|---|
Human | Expected |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 0.3-4 µg/mL | Notes Do not fix cells, see Menier et al. ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody. |
Select an associated product type
Isoform 1Non-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).Isoform 2Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).Isoform 3Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).Isoform 4Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).Isoform 5Non-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).Isoform 6Likely does not bind B2M and presents peptides.Isoform 7Likely does not bind B2M and presents peptides.
HLA G antigen, MHC class I antigen G, HLA-G, HLA-6.0, HLAG
Mouse Monoclonal HLAG antibody. Suitable for Flow Cyt and reacts with Human samples. Cited in 31 publications. Immunogen corresponding to Recombinant Full Length Protein corresponding to Human HLA-G.
HLA G antigen, MHC class I antigen G, HLA-G, HLA-6.0, HLAG
IgG1
Mouse
pH: 7.4
Preservative: 0.097% Sodium azide
Constituents: PBS
Liquid
Monoclonal
MEM-G/9
Affinity purification Protein A
Reacts with the native form of human HLA-G on the cell surface as well as with soluble HLA-G molecule in its beta 2-microglobulin associated form. Specificity was demonstrated with cells transfected with either full-length HLA-G and HLA-G1 complementary DNA. This antibody does not compete with a tested panel of other monoclonal antibodies to HLA-G. We have data to indicate that this antibody may not cross react with Mouse. However, this has not been conclusively tested and expression levels may vary in certain cell lines/tissues.
Blue Ice
1-2 weeks
+4°C
-20°C
Upon delivery aliquot
Avoid freeze / thaw cycle
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Flow cytometry analysis showing separation of HLA-G trasnfected LCL cells (red-filled) from K562 cells (black-dashed) stained using ab7758 (concentration in sample 0.3 ?g/ml, GAM APC).
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