InVivoMAb anti-mouse NKG2AB6

CloneCatalog #Category
16A11 BE0339InVivoMAb Antibodies
$150 - $3920 Login for Academic & Non-profit Pricing

About InVivoMAb anti-mouse NKG2AB6

The 16A11 monoclonal antibody reacts with NKG2A from C57BL/6 mice, the antibody does not react with BALB/c or 129 mouse strains. NKG2A, also known as CD159a is a type II transmembrane glycoprotein which belongs to the killer cell lectin-like receptor (KLR) family. NKG2A is expressed on NK cells, NKT cells, and activated CD8 T cells. NKG2A forms a disulfide-bonded heterodimer with CD94 that can bind to non-classical MHC class I antigen Qa-1 on target cells and inhibit NK cell activation.

InVivoMAb anti-mouse NKG2AB6 Specifications

Isotype Mouse IgG2b, κ
Immunogen C57BL/6 mouse CD94/NKG2A transfected CHO cells
Reported Applications
  • Flow cytometry
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
  • >95%
  • Determined by SDS-PAGE
Sterility 0.2 μM filtered
Production Purified from tissue culture supernatant in an animal free facility
Purification Protein A
RRID AB_2894759
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

Application References

InVivoMAb anti-mouse NKG2AB6

  • Flow cytometry

Vance, R. E., et al. (2002). “Implications of CD94 deficiency and monoallelic NKG2A expression for natural killer cell development and repertoire formation.” Proceedings of the National Academy of Sciences 99(2): 868-873. PubMed

Natural killer (NK) cells are believed to achieve self-tolerance through the expression of self-MHC-specific inhibitory receptors, such as members of the Ly49 and CD94/NKG2 families. Individual Ly49 genes are stochastically expressed by NK subsets and are expressed in a monoallelic fashion, but little is known about the mechanisms underlying CD94/NKG2A expression. We show here that, like Ly49 genes, mouse Nkg2a is stochastically and monoallelically expressed. Thus, a single general mechanism controls expression of all known MHC-specific receptors by mouse NK cells. In addition, we find that DBA/2J mice are naturally CD94-deficient and do not express cell-surface CD94/NKG2A receptors, even on neonatal NK cells. Thus, self-tolerance of neonatal NK cells cannot be attributed to CD94/NKG2A expression. Taken together, the results lead to a reconsideration of current models of NK cell development and self-tolerance.