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HLA-G (Major Histocompatibility Complex, class I, G) Antibody [HLAG/7749]

In Stock
Catalog Number Formulation Size Price
3135-MSM9-P0
Purified Ab with BSA and Azide at 200ug/ml
20ug
$229.00
3135-MSM9-P1
Purified Ab with BSA and Azide at 200ug/ml
100ug
$519.00
3135-MSM9-P1ABX
Purified Ab WITHOUT BSA and Azide at 1.0mg/ml
100ug
$519.00
Flat Rate Domestic: $60 | Orders outside the US - Contact Us for Order Information | Ships next business day

Applications & Dilutions

Applications Tested Dillution Protocol Note
Immunohistochemistry (IHC)
1-2ug/ml
30 min at RT. Staining of formalin-fixed tissues requires heating tissue sections in 10mM Tris with 1mM EDTA, pH 9.0, for 45 min at 95°C followed by cooling at RT for 20 minutes

Summary

Major histocompatibility complex (MHC), human leukocyte antigen (HLA) molecules are cell-surface receptors that bind foreign peptides and present them to T lymphocytes. MHC class I molecules consist of two polypeptide chains, an a or heavy chain, and a non-covalently associated protein, β2-microglobulin. Cytotoxic T lymphocytes bind antigenic peptides presented by MHC class I molecules. Antigens that bind to MHC class I molecules are typically 8-10 residues in length and are stabilized in a peptide binding groove. MHC class II molecules are encoded by polymorphic MHC genes and consist of a noncovalent complex of an a and b chain. Helper T lymphocytes bind antigenic peptides presented by MHC class II molecules. MHC class II molecules bind 13-18 amino acid antigenic peptides. Accumulating in endosomal/lysosomal compartments and on the surface of B cells, HLA-DM and -DO molecules regulate binding of exogenous peptides to class II molecules (HLA-DR) by sustaining a conformation that favors peptide exchange. The differential structural properties of MHC class I and class II molecules account for their respective roles in activating different populations of T lymphocytes.

Product Properties & Targets

Antibody Type
Host
Mouse
Applications
Species Reactivity
Isotype / Light Chain
IgG1 / Kappa
Cellular Localization
Cell surface.
Gene Name
Positive Control
Raji cells. Expressed in trophoblasts.
Immunogen
Recombinant fragment (around aa1-200) of human HLAG protein (exact sequence is proprietary)
Alternate Names
HLA class I histocompatibility antigen, alpha chain G | Soluble HLA class I histocompatibility antigen, alpha chain G, HLA G antigen, MHC class I antigen G, B2 microglobulin; DADB-15K14.8; HLA 6.0; HLA G histocompatibility antigen class I G; HLA G3; HLA60; HLAG; Major histocompatibility complex class I G; MHC class I antigen G; MHC G; T-cell A locus; TCA

Database Links

Entrez Gene ID
SwissProt

Additional Information

Clone
HLAG/7749
Chromosome Location
6p22.1
Mol. Weight of Antigen
39kDa

Functions

  • 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 pro-inflammatory 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).
  • Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).
  • Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).
  • Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).
  • 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 pro-inflammatory 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).
  • Likely does not bind B2M and presents peptides.
  • Likely does not bind B2M and presents peptides.

Key References

  • Babusikova O., et al. Neoplasma, 1985, 32(6):657-62.

PubMed Links

Storage & Stability

Antibody with azide - store at 2 to 8°C. Antibody without azide - store at -20 to -80°C.Antibody is stable for 24 months. Non-hazardous. No MSDS required.

Limitations

This antibody is available for research use only and is not approved for use in diagnosis.

Supplied as

200ug/ml of Ab purified from Bioreactor Concentrate by Protein A/G. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA & azide at 1.0mg/ml.

Warranty

There are no warranties, expressed or implied, which extend beyond this description. Company is not liable for any personal injury or economic loss resulting from this product.

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