Alexa Fluor® 488 Anti-HLA G antibody [5A6G7],Abcam,AB239342
Alexa Fluor® is a registered trademark of Molecular Probes, Inc, a Thermo Fisher Scientific Company. The Alexa Fluor® dye included in this product is provided under an intellectual property license from Life Technologies Corporation. As this product contains the Alexa Fluor® dye, the purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). As this product contains the Alexa Fluor® dye the sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: in manufacturing; (ii) to provide a service, information, or data in return for payment (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are sold for use in research. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, 5781 Van Allen Way, Carlsbad, CA 92008 USA or [email protected].
Host
Mouse
Application
Flow Cyt (Intra)
Conjugate
Alexa Fluor® 488
Platform ID
BAB531256812
Abcam
Contact
Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215
Email:
Specifications
Scientific Background
Target data 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).. 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 : 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 : 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). 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. See full target information HLA-G
Category Paths
- Products>Primary Antibodies>Monoclonal Antibodies
Please provide the required information below so that we can quickly source your products.