Anti-HLA-G antibody [MEM-G/11] {FITC} (STJ16100211)

SKU:
STJ16100211-01

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Host: Mouse
Applications: FC
Reactivity: Human
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Mouse monoclonal antibody anti-HLA-G is suitable for use in Flow Cytometry research applications.
Clonality: Monoclonal
Clone ID: MEM-G/11
Conjugation: FITC
Isotype: IgG1
Formulation: Phosphate buffered saline (PBS) solution with 15 mM sodium azide
Concentration: 1 mg/mL
Storage Instruction: Store at 2-8°C upon receipt.
Gene Symbol: HLA-G
Gene ID: 3135
Uniprot ID: HLAG_HUMAN
Immunogen: Recombinant human HLA-G refolded with beta2-microglobulin and peptide.
Post Translational Modifications N-glycosylated. Soluble HLA class I histocompatibility antigen, alpha chain G: Produced by proteolytic cleavage at the cell surface (shedding) by matrix metalloproteinase MMP2.
Function Isoform 1: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface. In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins. 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. 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. Through interaction with KIR2DL4 receptor on decidual macrophages induces pro-inflammatory cytokine production mainly associated with tissue remodeling. 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. 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. Reprograms B cells toward an immune suppressive phenotype via LILRB1. May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes. Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites. Isoform 2: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity. Isoform 3: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity. Isoform 4: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity. Isoform 5: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface. In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins. 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. 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. Through interaction with KIR2DL4 receptor on decidual macrophages induces pro-inflammatory cytokine production mainly associated with tissue remodeling. 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. Reprograms B cells toward an immune suppressive phenotype via LILRB1. Isoform 6: Likely does not bind B2M and presents peptides. Isoform 7: Likely does not bind B2M and presents peptides.
Protein Name Hla Class I Histocompatibility Antigen - Alpha Chain G
Hla G Antigen
Mhc Class I Antigen G Cleaved Into - Soluble Hla Class I Histocompatibility Antigen - Alpha Chain G
Shla-G
Database Links Reactome: R-HSA-1236974
Reactome: R-HSA-1236977
Reactome: R-HSA-198933
Reactome: R-HSA-877300
Reactome: R-HSA-909733
Reactome: R-HSA-9705671
Reactome: R-HSA-983170
Cellular Localisation Isoform 1: Cell Membrane
Single-Pass Type I Membrane Protein
Endoplasmic Reticulum Membrane
Early Endosome Membrane
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
Cell Projection
Filopodium Membrane
Hla-G Trogocytosis From Extravillous Trophoblast's Filopodia Occurs In The Majority Of Decidual Nk Cells
Alternative Antibody Names Anti-Hla Class I Histocompatibility Antigen - Alpha Chain G antibody
Anti-Hla G Antigen antibody
Anti-Mhc Class I Antigen G Cleaved Into - Soluble Hla Class I Histocompatibility Antigen - Alpha Chain G antibody
Anti-Shla-G antibody
Anti-HLA-G antibody
Anti-HLA-6.0 antibody
Anti-HLAG antibody

Information sourced from Uniprot.org

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