Alexa Fluor® 488 Anti-HLA G antibody [EPR23298-97],Abcam,AB300056

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 . 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 . 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

Rabbit

Reactivity

Human, Human

Application

IHC-P, ICC/IF

Conjugate

Alexa Fluor® 488

Platform ID

BAB843763059

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAlexa Fluor® 488 Anti-HLA G antibody [EPR23298-97]
Cat. No.AB300056
HostRabbit
IsotypeIgG
ReactivityHuman, Human
ConjugationAlexa Fluor® 488
ApplicationIHC-P, ICC/IF
ClonalityMonoclonal
Clone NumberEPR23298-97
Concentration0.5 mg/mL Batch dependent concentration
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Storage-20°C
Regulatory StatusResearch Use Only

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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