Human KIR3DL1 Alexa Fluor® 750-conjugated Antibody Summary
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
KIR3DL1 (3DL1, previously called NKB1 or NKAT3, designated CD158e) is a 70 kDa type I transmembrane glycoprotein that belongs to the killer cell Ig-like receptor (KIR) family. KIRs are expressed on CD56dim NK cells and T cell subsets where they 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. Like other inhibiting KIRs, KIR3DL1 has two ITIM domains within its long tail (2). The 319 amino acid (aa) ECD of KIR3DL1 shows 97% aa identity with an activating KIR, KIR3DS1, and the two segregate as alleles (3, 4). KIR3DL1 binds to HLA antigens. This includes HLA-A and -B molecules. Among the HLA-B variants, only the Bw4 epitope, which is present within only one third of all HLA-B alleles, is recognized by KIR3DL1 (4). An NK cell expressing KIR3DL1 is prevented from killing a cell expressing the Bw4 epitope on its surface. However, if the epitope is downregulated on the cell surface due to viral infection, the NK cell is released from inhibition and now kills the infected cell. KIR genes are highly polymorphic, and specific KIR3DL1 alleles vary in surface expression and activity. For example, the allele KIR3DL1*004 is associated with slow progression to AIDS in HIV infected individuals that also express Bw4 (6). Unlike most alleles that are surface-expressed, this allele is mainly retained within the cell (7). KIR3DL1/S1 is the only KIR receptor to have an ortholog in non-primates, including selected mouse strains in which it is also called KIRL1 (KIR-like 1). Although the ECD of human KIR3DL1 shares 40‑48% aa identity with mouse, rat and bovine KIR3DL1, the transmembrane and cytoplasmic regions in the non-primate species show no obvious activating or inhibiting motifs (8, 9).
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- Lanier, L. L. (2005) Annu. Rev. Immunol. 23:225.
- Uhrberg, M. et al. (1997) Immunity 7:753.
- O’Connor, G. M. et al. (2007) J. Immunol. 178:235.
- Thananchai, H. et al. (2007) J. Immunol. 178:33.
- Martin, M.P. et al. (2007) Nat. Genet. 39:733.
- Pando, M.J. et al. (2003) J. Immunol. 171:6640.
- Hoelsbrekken, S.E. et al. (2003) J. Immunol. 170:2259.
- Wilson, E.B. et al. (2007) Immunogenetics 59:641.
Product Specific Notices
This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.
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