• Purity

  >95%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

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

• Activity

  Measured by its ability to bind BJAB human Burkitt's lymphoma cells in a flow cytometry assay. Katz, G.     et al. (2001) J. Immunol.     166:7260. Ishido, S.     et al. (2000) Immunity     13:365.

  When 100 ng of Recombinant Human KIR2DS4/CD158i Fc Chimera is added to 2 x 10⁵ BJAB cells, >30% of the cells will bind to the protein.

• Source

  Mouse myeloma cell line, NS0-derived

  Human KIR2DS4 (Gln22 - His245) Accession # P43632	IEGRMD	Human IgG1 (Pro100 - Lys330)
  N-terminus		C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  No results obtained: Gln22 predicted    
   

• Predicted Molecular Mass

  51.2 kDa (monomer)

• SDS-PAGE

  70-85 kDa, reducing conditions

Background: KIR2DS4/CD158i

KIR2DS4 (2DS4), previously called NKAT-8 and designated CD158i, is a type I transmembrane glycoprotein that belongs to the killer cell Ig-like receptor (KIR) family (1). KIRs are expressed on CD56^dim NK cells and T cell subsets where they differentiate normal from abnormal cells and regulate effector functions in the innate immune system (1 ‑ 3). KIRs are named for the number of Ig-like domains (2D or 3D) in the extracellular domain (ECD), and whether they have long or short (L, S) cytoplasmic tails. KIR2DS4 cDNA encodes 304 amino acids (aa) including a 21 aa signal sequence, a 224 aa ECD, a 20 aa transmembrane sequence and a 39 aa cytoplasmic domain. KIR receptors have no structural orthologs in nonprimates, although mouse Ly-49 proteins perform similar functions (2). Like other activating KIRs, KIR2DS4 has a short tail and a positively charged amino acid (aa) within the transmembrane domain that interacts with the ITAM-bearing signaling adaptor, DAP12 (2, 3). Expression of activating KIR is balanced with inhibitory KIR to impart specificity to the immune response. KIR2DS4 recognizes six HLA-C allotypes and two HLA-A allotypes (A*1101 and A*1102) but no HLA-B allotypes (4, 5). It has also been suggested that KIR2DS4 recognizes a non-MHC ligand, based on specific binding to melanoma cells that lack MHC Class I (6). A common allele, KIR2DS4*003, is present in up to 89% of Caucasians and ~30% of Asians; it creates a prematurely terminated, soluble, inactive form (7, 8). Lack of functional KIR2DS4 can potentially create unbalanced inhibition of killer cell function (4, 8).

• References:

1. Bottino, C. et al. (1996) Eur. J. Immunol. 26:1816.

2. Lanier, L. L. (2005) Annu. Rev. Immunol. 23:225.

3. Purdy, A.K. and K.S. Campbell (2009) Cancer Biol. Ther. 8:13.

4. Graef, T. et al. (2009) J. Exp. Med. 206:2557.

5. Katz, G. et al. (2001) J. Immunol. 166:7260.

6. Katz, G. et al. (2004) J. Immunol. 173:1819.

7. Maxwell, L.D. et al. (2004) Hum. Immunol. 65:613.

8. Middleton, D. et al. (2007) Hum. Immunol. 68:128.

• Long Name:

  Killer Cell Immunoglobulin-like Receptor, Two Domains, Short Cytoplasmic Tail, 4

• Entrez Gene IDs:

  3809 (Human)

• Alternate Names:

  CD158 antigen-like family member I; CD158i antigen; CD158i; cl-39; killer cell immunoglobulin-like receptor 2DS4; killer cell immunoglobulin-like receptor, two domains, short cytoplasmic tail4,nkat8; killer inhibitory receptor 4-1-2; KIR antigen 2DS4; KIR2DS4; KKA3KIR1D; MGC120019; MGC125315; MGC125317; MHC class I NK cell receptor; natural killer cell inhibitory receptor; Natural killer-associated transcript 8; NKAT-8; NKAT8KIR412; P58 natural killer cell receptor clones CL-39/CL-17; p58 NK receptor CL-39/CL-17