• Purity

  >95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.

• Endotoxin Level

  <0.10 EU per 1 μg of the protein by the LAL method.  

• Activity

  Measured by its binding ability in a functional ELISA. When Recombinant Mouse NKG2A/CD159a Fc Chimera is coated at 0.5 µg/mL, recombinant human CD94 binds with a typical ED    ₅₀ of    
  0.1-0.6 μg/mL.

• Source

  Chinese Hamster Ovary cell line, CHO-derived

  MDP	Mouse IgG2A (Glu98-Lys330)	IEGR	Mouse NKG2A (Ala94-IIe244) Accession # Q9Z202
  N-terminus			C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  Met

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  44 kDa

• SDS-PAGE

  58-67 kDa, reducing conditions

Data Images

Background: NKG2A/CD159a

NKG2A/CD159a is an approximately 40 kDa transmembrane C-type lectin superfamily protein that inhibits innate immune system activation (1). Mouse NKG2A consists of a 70 amino acid (aa) cytoplasmic domain with two ITIM inhibitory motifs, a 23 aa transmembrane segment, and a 151 aa extracellular domain (ECD) with one C-type lectin domain (2). Within the ECD, mouse NKG2A shares 41% and 71% aa sequence identity with human and rat NKG2A, respectively. Alternative splicing generates additional isoforms with a 17 aa deletion in the extracellular juxtamembrane region or a substitution of that region plus the transmembrane segment. NKG2A is expressed on a subset of NK cells and CD8  ⁺ T cells (2-6) where it forms a covalent heterodimer with CD94 (5, 7, 8). NKG2A-CD94 heterodimers bind to the widely expressed nonclassical MHC-I molecule, HLA-E (Qa-1  ^b in mouse), which presents a peptide derived from the signal peptide of classical MHC-I molecules (2, 7). Triggering the NKG2A-CD94 complex inhibits the cytolytic activity of NK and CD8  ⁺ T cells (2, 3, 5, 6, 9). This enables the innate immune system to detect cells that express host MHC-I molecules and to protect them from NK cell mediated lysis. This mechanism is subverted by human cytomegalovirus which encodes a peptide that is homologous to the HLA-E binding peptide (10). HCMV infected cells up-regulate both HLA-E and NKG2A expression and utilize this peptide to escape from immune clearance (3, 10). In contrast, vaccinia virus induces HLA-E down-regulation, thus permitting NK cell lysis of the virally infected cell (11).

• References:

1. Das, J. and S.I. Khakoo (2015) Immunol. Rev. 267:214.

2. Vance, R.E. et al. (1998) J. Exp. Med. 188:1841.

3. Saez-Borderias, A. et al. (2009) J. Immunol.182:829.

4. Houchins, J.P. et al. (1997) J. Immunol. 158:3603.

5. Brooks, A.G. et al. (1997) J. Exp. Med. 185:795.

6. Zhou, J. et al. (2008) J. Immunol. 180:25.

7. Braud, V.M. et al. (1998) Nature 391:795.

8. Carretero, M. et al. (1997) Eur. J. Immunol. 27:563.

9. Lee, N. et al. (1998) Proc. Natl. Acad. Sci. USA 95:5199.

10. Tomasec, P. et al. (2000) Science 287:1031.

11. Brooks, C.R. et al. (2006) J. Immunol. 176:1141.

• Long Name:

  Natural Killer G2A

• Entrez Gene IDs:

  3821 (Human); 16641 (Mouse)

• Alternate Names:

  CD159 antigen-like family member A; CD159a antigen; CD159a; C-lectin type II protein; killer cell lectin-like receptor subfamily C, member 1; Klrc1; MGC13374; natural killer cell lectin; natural killer group protein 2; NK cell receptor A; NKG2; NKG2-1/B activating NK receptor; NKG2A; NKG2-A; NKG2-A/B type II integral membrane protein; NKG2-A/B-activating NK receptor; NKG2-A/NKG2-B type II integral membrane protein; NKG2AMGC59791; NKG2-B