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> home > Products > Primary Antibodies > Antibody Collections > Recombinant Antibodies > Anti-NKG2A / CD94 Reference Antibody (monalizumab)
Anti-NKG2A / CD94 Reference Antibody (monalizumab)
Recombinant Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| FC, E, FTA |
|---|---|
| Primary Accession | P26715 |
| Reactivity | Baboon, Cynomolgus, Human |
| Clonality | Monoclonal |
| Isotype | IgG4 |
| Calculated MW | 145 KDa |
| Target/Specificity | NKG2A / CD94 |
|---|---|
| Endotoxin | < 0.001EU/ µg,determined by LAL method. |
| Conjugation | Unconjugated |
| Expression system | CHO Cell |
| Format | Purified monoclonal antibody supplied in PBS, pH6.0, without preservative.This antibody is purified through a protein A column. |
| Name | KLRC1 |
|---|---|
| Synonyms | NKG2A {ECO:0000303|PubMed:18083576} |
| 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 (PubMed:18083576, PubMed:37264229, PubMed:9430220, PubMed:9486650). 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 (PubMed:12165520, PubMed:9485206). Key inhibitory receptor on natural killer (NK) cells that regulates their activation and effector functions (PubMed:30860984, PubMed:9430220, PubMed:9485206, PubMed:9486650). 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 (PubMed:12387742). 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 (PubMed:18064301). 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 (PubMed:30503213, PubMed:30860984). |
| Cellular Location | Cell membrane; Single-pass type II membrane protein |
| Tissue Location | Predominantly expressed in NK cells (at protein level) (PubMed:20952657, PubMed:9430220, PubMed:9485206). Expressed in intraepithelial CD8-positive T cell subsets with higher frequency in gamma-delta T cells than alpha-beta T cells (at protein level) (PubMed:18064301). Expressed in memory gamma-delta T cells (at protein level) (PubMed:20952657). Restricted to a subset of memory/effector CD8-positive alpha-beta T cells (at protein level) (PubMed:12387742) Expressed in intratumoral NK and CD8-positive T cells (PubMed:30503213). Expressed in melanoma-specific cytotoxic T cell clones (at protein level) (PubMed:9485206). 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) (PubMed:20952657). |
Research Areas
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$ 365.00
Cat# APR10416
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