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Your Position: > Protein > NKG2A > NKA-H5244

Human NKG2A / CD159a Protein, His Tag

  • Synonym
    NKG2A,CD159a,KLRC1,NK cell receptor A
  • Source
    Human NKG2A, His Tag(NKA-H5244) is expressed from human 293 cells (HEK293). It contains AA Pro 94 - Leu 233 (Accession # P26715-1).
    Predicted N-terminus: His
  • Molecular Characterization
    NKG2A Structure

    This protein carries a polyhistidine tag at the N-terminus.

    The protein has a calculated MW of 17.9 kDa. The protein migrates as 30-40 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

  • Endotoxin
    Less than 1.0 EU per μg by the LAL method.
  • Purity

    >90% as determined by SDS-PAGE.

  • Formulation

    Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

    Contact us for customized product form or formulation.

  • Reconstitution

    Please see Certificate of Analysis for specific instructions.

    For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

  • Storage

    For long term storage, the product should be stored at lyophilized state at -20°C or lower.

    Please avoid repeated freeze-thaw cycles.

    This product is stable after storage at:

    1. -20°C to -70°C for 12 months in lyophilized state;
    2. -70°C for 3 months under sterile conditions after reconstitution.
SDS-PAGE
NKG2A SDS-PAGE

Human NKG2A, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90% (With Star Ribbon Pre-stained Protein Marker).

  • Background
    NKG2A/CD159a is a transmembrane protein belonging to the CD94/NKG2 family of C-type lectin-like receptors that inhibits innate immune system activation, also known as KLRC1, CD159a, NK cell receptor A and NKG2-A/NKG2-B type II integral membrane protein. NKG2A marks a unique immune effector subset preferentially co-expressing the tissue-resident CD103 molecule, but not immune checkpoint inhibitors. NKG2A blockade therapy operated through CD8 T cells, but not NK cells. The increase in NKG2A expression might be induced by IL-10, which was present at a high level in the plasma of HCC patients. Blocking IL-10 could specifically inhibit NKG2A expression in NK cells. These findings indicate that NKG2A expression is influenced by factors from cancer nests and contributes to NK cell exhaustion, suggesting that NKG2A blockade has the potential to restore immunity against liver tumors by reversing NK cell exhaustion.
  • Clinical and Translational Updates

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