Human KIR3DL2/CD158k Alexa Fluor® 405-conjugated Antibody Summary
Accession # P43630
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
KIR3DL2 (3DL2, p140, CD158k) is a type I transmembrane protein of the p70 family of killer cell Ig-like receptors (KIR). KIR are expressed on CD56dim NK cells and T cell subsets where they participate in identifying normal and abnormal cells and regulating effector functions of the innate immune system (1-4). KIR 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 inhibitory KIR, KIR3DL2 has two ITIM domains within its long tail (3). KIR3DL2 is diverse, with twelve alleles identified and as many as five single amino acid polymorphisms found in a single individual (4-6). Unlike most other KIR, gene transcripts of KIR3DL2 are expressed by all individuals (4). KIR3DL2 is present on the cell surface as a disulfide-linked homodimer of 70 kDa, 434 aa subunits (4). KIR3DL2 has shown peptide-specific binding to some HLA-A antigens, including A3 and A11 (4, 7, 8). It also binds the abnormally folded HLA-B27 homodimer found in spondylarthritides, but not the normal heterodimer of HLA-B27 with beta 2‑microglobulin (9, 10). NK and CD4+ T cells from patients with spondylarthritides show increased KIR3DL2+ expression and may play a role in disease pathology (10). KIR3DL2 is also a marker for atypical mononuclear (Sezary) cells in the blood of patients with Sezary syndrome, an erythrodermic form of cutaneous T cell lymphoma (11). Human KIR3DL2 ECD shows 88-92% aa identity to KIR3DL2 of other primates. KIR receptors have no structural orthologs in non-primates, although mouse Ly-49 proteins are functional orthologs (3). KIR are highly related. The closest relative, KIR3DL1 shows 86% aa identity with KIR3DL2 within the ECD.
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Product Specific Notices
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