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http://purl.uniprot.org/citations/19858347http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19858347http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19858347http://www.w3.org/2000/01/rdf-schema#comment"Human killer cell immunoglobulin-like receptors (KIRs) are distinguished by expansion of activating KIR2DS, whose ligands and functions remain poorly understood. The oldest, most prevalent KIR2DS is KIR2DS4, which is represented by a variable balance between "full-length" and "deleted" forms. We find that full-length 2DS4 is a human histocompatibility leukocyte antigen (HLA) class I receptor that binds specifically to subsets of C1+ and C2+ HLA-C and to HLA-A*11, whereas deleted 2DS4 is nonfunctional. Activation of 2DS4+ NKL cells was achieved with A*1102 as ligand, which differs from A*1101 by unique substitution of lysine 19 for glutamate, but not with A*1101 or HLA-C. Distinguishing KIR2DS4 from other KIR2DS is the proline-valine motif at positions 71-72, which is shared with KIR3DL2 and was introduced by gene conversion before separation of the human and chimpanzee lineages. Site-directed swap mutagenesis shows that these two residues are largely responsible for the unique HLA class I specificity of KIR2DS4. Determination of the crystallographic structure of KIR2DS4 shows two major differences from KIR2DL: displacement of contact loop L2 and altered bonding potential because of the substitutions at positions 71 and 72. Correlation between the worldwide distributions of functional KIR2DS4 and HLA-A*11 points to the physiological importance of their mutual interaction."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.org/dc/terms/identifier"doi:10.1084/jem.20091010"xsd:string
http://purl.uniprot.org/citations/19858347http://purl.org/dc/terms/identifier"doi:10.1084/jem.20091010"xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Parham P."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Parham P."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Bushnell D.A."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Bushnell D.A."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Robinson P.J."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Robinson P.J."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Norman P.J."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Norman P.J."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Hammond J.A."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Hammond J.A."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Abi-Rached L."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Abi-Rached L."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Guethlein L.A."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Guethlein L.A."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Gleimer M."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Gleimer M."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Graef T."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Graef T."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Moesta A.K."xsd:string
http://purl.uniprot.org/citations/19858347http://purl.uniprot.org/core/author"Moesta A.K."xsd:string