Human NKG2-2A/KLRC1/CD159a protein (Recombinant) (N-His&Avi) {Biotin} (STJP020198)
SPECIFICATIONS
HostHEK293 cells
ConjugationBiotin
ImmunogenBiotinylated Recombinant Human NKG2-2A/KLRC1/CD159a Protein is produced by Expi293 expression system. The target protein is expressed with sequence (Arg100-Leu233) of Human NKG2-2A fused with a His tag and Avi tag at the N-terminal.
General Information
| Short Description | Recombinant-Human NKG2-2A/KLRC1/CD159a-N-His&Avi protein was developed in hek293 cells using the region Arg100-Leu233. For use in research applications. |
| Host | HEK293 cells |
| Note | STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
Product Properties
| Conjugation | Biotin |
| Formulation | Lyophilised from a 0.22 Mu m filtered solution of PBS, pH 7.4. |
| Storage Instruction | Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles. |
| Determination Method | < 1 EU/Mu g of the protein by LAL method. |
Target Information
| Gene Symbol | KLRC1 |
| Gene ID | 3821 |
| Uniprot ID | NKG2A_HUMAN |
| Immunogen | Biotinylated Recombinant Human NKG2-2A/KLRC1/CD159a Protein is produced by Expi293 expression system. The target protein is expressed with sequence (Arg100-Leu233) of Human NKG2-2A fused with a His tag and Avi tag at the N-terminal. |
| Immunogen Region | Arg100-Leu233 |
Additional Info
| Tissue Specificity | Predominantly expressed in NK cells (at protein level). Expressed in intraepithelial CD8-positive T cell subsets with higher frequency in gamma-delta T cells than alpha-beta T cells (at protein level). Expressed in memory gamma-delta T cells (at protein level). Restricted to a subset of memory/effector CD8-positive alpha-beta T cells (at protein level). Expressed in intratumoral NK and CD8-positive T cells. Expressed in melanoma-specific cytotoxic T cell clones (at protein level). KLRD1-KLRC1 and KLRD1-KLRC2 are differentially expressed in NK and T cell populations, with only minor subsets expressing both receptor complexes (at protein level). |
| Post Translational Modifications | Phosphorylated. |
| Function | Immune inhibitory receptor involved in self-nonself discrimination. In complex with KLRD1 on cytotoxic and regulatory lymphocyte subsets, recognizes non-classical major histocompatibility (MHC) class Ib molecule HLA-E loaded with self-peptides derived from the signal sequence of classical MHC class Ia molecules. Enables cytotoxic cells to monitor the expression of MHC class I molecules in healthy cells and to tolerate self. Upon HLA-E-peptide binding, transmits intracellular signals through two immunoreceptor tyrosine-based inhibition motifs (ITIMs) by recruiting INPP5D/SHP-1 and INPPL1/SHP-2 tyrosine phosphatases to ITIMs, and ultimately opposing signals transmitted by activating receptors through dephosphorylation of proximal signaling molecules. Key inhibitory receptor on natural killer (NK) cells that regulates their activation and effector functions. Dominantly counteracts T cell receptor signaling on a subset of memory/effector CD8-positive T cells as part of an antigen-driven response to avoid autoimmunity. On intraepithelial CD8-positive gamma-delta regulatory T cells triggers TGFB1 secretion, which in turn limits the cytotoxic programming of intraepithelial CD8-positive alpha-beta T cells, distinguishing harmless from pathogenic antigens. In HLA-E-rich tumor microenvironment, acts as an immune inhibitory checkpoint and may contribute to progressive loss of effector functions of NK cells and tumor-specific T cells, a state known as cell exhaustion. (Microbial infection) Viruses like human cytomegalovirus have evolved an escape mechanism whereby virus-induced down-regulation of host MHC class I molecules is coupled to the binding of viral peptides to HLA-E, restoring HLA-E expression and inducing HLA-E-dependent NK cell immune tolerance to infected cells. Recognizes HLA-E in complex with human cytomegalovirus UL40-derived peptide (VMAPRTLIL) and inhibits NK cell cytotoxicity. (Microbial infection) May recognize HLA-E in complex with HIV-1 gag/Capsid protein p24-derived peptide (AISPRTLNA) on infected cells and may inhibit NK cell cytotoxicity, a mechanism that allows HIV-1 to escape immune recognition. (Microbial infection) Upon SARS-CoV-2 infection, may contribute to functional exhaustion of cytotoxic NK cells and CD8-positive T cells. On NK cells, may recognize HLA-E in complex with SARS-CoV-2 S/Spike protein S1-derived peptide (LQPRTFLL) expressed on the surface of lung epithelial cells, inducing NK cell exhaustion and dampening antiviral immune surveillance. |
| Protein Name | Nkg2-A/Nkg2-B Type Ii Integral Membrane ProteinCd159 Antigen-Like Family Member ANk Cell Receptor ANkg2-A/B-Activating Nk ReceptorCd Antigen Cd159a |
| Database Links | Reactome: R-HSA-198933 |
| Cellular Localisation | Cell MembraneSingle-Pass Type Ii Membrane Protein |
| Alternative Protein Names | Nkg2-A/Nkg2-B Type Ii Integral Membrane Protein proteinCd159 Antigen-Like Family Member A proteinNk Cell Receptor A proteinNkg2-A/B-Activating Nk Receptor proteinCd Antigen Cd159a proteinKLRC1 proteinNKG2A protein |
Information sourced from Uniprot.org