Anti-HLA G antibody [EPR23298-97] - BSA and Azide free,Abcam,AB283278
What is this antibody validated in? Anti-HLA G antibody [EPR23298-97] - BSA and Azide free (ab283278) is a rabbit recombinant monoclonal antibody and is validated for use in Western Blot (WB), Immunohistochemistry (IHC-P), Immunocytochemistry/immunofluorescence (ICC/IF) in Human samples. What is the molecular weight of HLA G? Anti-HLA G [EPR23298-97] - BSA and Azide free (ab283278) specifically detects a band for HLA G (UniProt: P17693) at a molecular weight of 38kDa. Other related products We have a range of other formats of antibody clone [EPR23298-97] also available for your convenience: ab283260 , Carrier free - ab283278, Alexa Fluor® 488 - ab300056 Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents . What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including: - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies . Conjugation ready Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications. Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold. Compatibility This product is compatible with the Maxpar ® Antibody Labeling Kit from Fluidigm, without the need for antibody preparation. Maxpar ® is a trademark of Fluidigm Canada Inc.
Host
Rabbit
Reactivity
Human
Application
WB, IHC-P, ICC/IF
Platform ID
BAB709970988
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
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- Products>Primary Antibodies>IHC Antibodies
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