Monkey Soluble Leukocyte antigen G ELISA Kit (RMEK-0153423)
Cat. No.: RMEK-0153423
Category: ELISA Kits
INQUIRY
1 x 96 tests
This ELISA kit is a 1. 5 hour solid-phase ELISA designed for the quantitative determination of the targets. This ELISA kit for research use only, not for therapeutic or diagnostic applications!
Product Features
| Species Reactivity | Monkey |
|---|---|
| Assay Time | 1.5 h |
Target Information
| Target Symbol | sHLA G |
|---|---|
| UniProt ID | P17693 |
| 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. |
| Cellular Localization | [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; Single-pass type I membrane protein. [Isoform 3]: Cell membrane; Single-pass type I membrane protein. [Isoform 4]: Cell membrane; Single-pass type I membrane protein. [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. |
| Development Stage | Expressed at the morula stage (at protein level). Expressed in extravillous trophoblast and cytotrophoblast. Expressed in fetal eye and thymus. [Isoform 7]: Expressed in fetal liver. |
| Domain | The VL9 peptide/epitope (VMAPRTLFL) derived from the signal sequence is loaded onto HLA-E and enables HLA-E expression at the plasma membrane. Confers strong recognition by KLRD1-KLRC1 or KLRD1-KLRC2 receptors on NK cells. |
| Post-transcriptional 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. |
Storage & Shipping
| Storage | Store at 2-8°C |
|---|---|
| Shipping | Gel Packs |
| Stability | The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. |
For research use only. Not for clinical use.
