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>   首页   >   产品   >   一抗   >   免疫学   >   HLA-G Antibody   

HLA-G Antibody

Purified Rabbit Polyclonal Antibody (Pab)

     
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB
Primary Accession P17693
Reactivity Human, Mouse, Rat
Host Rabbit
Clonality Polyclonal
Calculated MW 38224 Da
Additional Information
Gene ID 3135
Other Names HLA class I histocompatibility antigen, alpha chain G, HLA G antigen, MHC class I antigen G, HLA-G, HLA-60, HLAG
Dilution WB~~1:1000
Format 0.01M PBS, pH 7.2, 0.09% (W/V) Sodium azide, Glycerol 50%
StorageStore at -20 °C.Stable for 12 months from date of receipt
Protein Information
Name HLA-G {ECO:0000303|PubMed:1570318, ECO:0000312|HGNC:HGNC:4964}
Function [Isoform 1]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed:19304799, PubMed:23184984, PubMed:29262349). 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:16366734, PubMed:19304799, PubMed:20448110, PubMed:23184984, PubMed:27859042, PubMed:29262349). 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:16366734, PubMed:19304799, PubMed:23184984, PubMed:29262349). 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).
Cellular Location [Isoform 1]: Cell membrane; Single-pass type I membrane protein. Endoplasmic reticulum membrane. Early endosome membrane [Isoform 2]: Cell membrane; Single-pass type I membrane protein [Isoform 4]: Cell membrane; Single-pass type I membrane protein [Isoform 6]: Secreted Cell projection, filopodium membrane. Note=HLA-G trogocytosis from extravillous trophoblast's filopodia occurs in the majority of decidual NK cells.
Tissue Location Expressed in adult eye (PubMed:1570318). Expressed in immune cell subsets including monocytes, myeloid and plasmacytoid dendritic cells and regulatory T cells (Tr1)(at protein level) (PubMed:20448110). Secreted by follicular dendritic cell and follicular helper T cells (PubMed:24453251) [Isoform 7]: Expressed in placenta, amniotic membrane, skin, cord blood and peripheral blood mononuclear cells
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

Involved in the presentation of foreign antigens to the immune system. Plays a role in maternal tolerance of the fetus by mediating protection from the deleterious effects of natural killer cells, cytotoxic T-lymphocytes, macrophages and mononuclear cells.

REFERENCES

Shukla H.,et al.Nucleic Acids Res. 18:2189-2189(1990).
Geraghty D.E.,et al.Proc. Natl. Acad. Sci. U.S.A. 84:9145-9149(1987).
Ishitani A.,et al.Submitted (APR-1992) to the EMBL/GenBank/DDBJ databases.
Hampe A.,et al.DNA Seq. 10:263-299(1999).
Shiina S.,et al.Submitted (SEP-1999) to the EMBL/GenBank/DDBJ databases.

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