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Mouse Anti-HLA-G Monoclonal Antibody (CBFYH-3144) (CBMAB-H0043-FY)

This product is mouse antibody that recognizes HLA-G. The antibody CBFYH-3144 can be used for immunoassay techniques such as: WB.
See all HLA-G antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYH-3144
Antibody Isotype
IgG1
Application
WB

Basic Information

Immunogen
Purified His-tagged HLA-G protein was used to produced this monoclonal antibody
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS
Preservative
0.09% Sodium azide
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
HLA-G
Introduction
HLA-G belongs to the HLA class I heavy chain paralogues. This class I molecule is a heterodimer consisting of a heavy chain and a light chain (beta-2 microglobulin). The heavy chain is anchored in the membrane. HLA-G is expressed on fetal derived placental cells. The heavy chain is approximately 45 kDa and its gene contains 8 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the alpha1 and alpha2 domain, which both bind the peptide, exon 4 encodes the alpha3 domain, exon 5 encodes the transmembrane region, and exon 6 encodes the cytoplasmic tail.
Entrez Gene ID
UniProt ID
Alternative Names
Major Histocompatibility Complex, Class I, G; HLA-G Histocompatibility Antigen, Class I, G; MHC Class I Antigen G; B2 Microglobulin; HLA G Antigen; HLA Class I Histocompatibility Antigen, Alpha Chain G
Function
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).

Isoform 2:
Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).

Isoform 3:
Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).

Isoform 4:
Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).

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).

Isoform 6:
Likely does not bind B2M and presents peptides.

Isoform 7:
Likely does not bind B2M and presents peptides.
Biological Process
Antigen processing and presentation of endogenous peptide antigen via MHC class Ib Source: UniProtKB
Antigen processing and presentation of peptide antigen via MHC class I Source: UniProtKB-KW
Cellular defense response Source: ProtInc
Immune response-inhibiting cell surface receptor signaling pathway Source: BHF-UCL
Negative regulation of angiogenesis Source: UniProtKB
Negative regulation of dendritic cell differentiation Source: BHF-UCL
Negative regulation of G0 to G1 transition Source: UniProtKB
Negative regulation of immune response Source: UniProtKB
Negative regulation of natural killer cell mediated cytotoxicity Source: UniProtKB
Negative regulation of protein kinase B signaling Source: UniProtKB
Negative regulation of T cell mediated cytotoxicity Source: UniProtKB
Negative regulation of T cell proliferation Source: BHF-UCL
Peripheral B cell tolerance induction Source: UniProtKB
Positive regulation of cellular senescence Source: UniProtKB
Positive regulation of endothelial cell apoptotic process Source: UniProtKB
Positive regulation of interleukin-12 production Source: BHF-UCL
Positive regulation of macrophage cytokine production Source: UniProtKB
Positive regulation of natural killer cell cytokine production Source: UniProtKB
Positive regulation of regulatory T cell differentiation Source: BHF-UCL
Positive regulation of T cell tolerance induction Source: BHF-UCL
Positive regulation of tolerance induction Source: UniProtKB
Protection from natural killer cell mediated cytotoxicity Source: UniProtKB
Protein homotrimerization Source: UniProtKB
Cellular Location
Isoform 1: Cell membrane; Early endosome membrane; Endoplasmic reticulum membrane
Chain Soluble HLA class I histocompatibility antigen, alpha chain G: Secreted
Isoform 2: Cell membrane
Isoform 3: Cell membrane
Isoform 4: Cell membrane
Isoform 5: Secreted; Early endosome
Isoform 6: Secreted
Isoform 7: Secreted; Filopodium membrane. HLA-G trogocytosis from extravillous trophoblast's filopodia occurs in the majority of decidual NK cells.
Topology
Extracellular: 25-308
Helical: 309-332
Cytoplasmic: 333-338
PTM
N-glycosylated.
Soluble HLA class I histocompatibility antigen, alpha chain G:
Produced by proteolytic cleavage at the cell surface (shedding) by matrix metalloproteinase MMP2.
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For research use only. Not intended for any clinical use.

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