anti-KIR2DL4/CD158d Antibody from antibodies-online

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antibodies-online for
anti-KIR2DL4/CD158d Antibody

Description

Product Characteristics: CD158d / KIR2DL4 is a KIR family member that shares structural features with both activating and inhibitory receptors and may mediate different functions under different circumstances. It contains cytoplasmic ITIM, suggesting inhibitory function, but also transmembrane domain similar to those of activating KIRs. It has been reported that CD158d serves as an inhibitory receptor for peripheral and uterine NK cells, but its ligation with soluble mAbs (unlike immobilized mAbs) results in activation of IFN-γ, secretion. CD158d also binds both membrane form and soluble form of its ligand HLA-G.
Target Information: 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. This gene is one of the 'framework' loci that is present on all haplotypes. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jul 2008]