|Other Names||Killer cell immunoglobulin-like receptor 2DS5, CD158 antigen-like family member G, MHC class I NK cell receptor, Natural killer-associated transcript 9, NKAT-9, CD158g, KIR2DS5, CD158G, NKAT9|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Receptor on natural killer (NK) cells for HLA-C alleles. Does not inhibit the activity of NK cells.|
|Cellular Location||Cell membrane; Single-pass type I membrane protein|
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Killer cell immunoglobulin-like receptors (KIRs) are transmembrane glycoproteins expressed by natural killer cells and subsets of T cells. The KIR genes are polymorphic and highly homologous and they are found in a cluster on chromosome 19q13.4 within the 1 Mb leukocyte receptor complex (LRC). The gene content of the KIR gene cluster varies among haplotypes, although several 'framework' genes are found in all haplotypes (KIR3DL3, KIR3DP1, KIR3DL4, KIR3DL2). The KIR proteins are classified by the number of extracellular immunoglobulin domains (2D or 3D) and by whether they have a long (L) or short (S) cytoplasmic domain. KIR proteins with the long cytoplasmic domain transduce inhibitory signals upon ligand binding via an immune tyrosine-based inhibitory motif (ITIM), while KIR proteins with the short cytoplasmic domain lack the ITIM motif and instead associate with the TYRO protein tyrosine kinase binding protein to transduce activating signals. The ligands for several KIR proteins are subsets of HLA class I molecules; thus, KIR proteins are thought to play an important role in regulation of the immune response.
Vilches, C., et al. Tissue Antigens 56(5):453-456(2000)Bottino, C., et al. Eur. J. Immunol. 26(8):1816-1824(1996)Dohring, C., et al. Immunogenetics 44(3):227-230(1996)Wagtmann, N., et al. Immunity 2(5):439-449(1995)
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