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Crystal structure of a lectin-like natural killer cell receptor bound to its MHC class I ligand
- Source :
- Nature. 402(6762)
- Publication Year :
- 1999
-
Abstract
- Natural killer (NK) cell function is regulated by NK receptors that interact with MHC class I (MHC-I) molecules on target cells. The murine NK receptor Ly49A inhibits NK cell activity by interacting with H-2D(d) through its C-type-lectin-like NK receptor domain. Here we report the crystal structure of the complex between the Ly49A NK receptor domain and unglycosylated H-2D(d). The Ly49A dimer interacts extensively with two H-2D(d) molecules at distinct sites. At one interface, a single Ly49A subunit contacts one side of the MHC-I peptide-binding platform, presenting an open cavity towards the conserved glycosylation site on the H-2D(d) alpha2 domain. At a second, larger interface, the Ly49A dimer binds in a region overlapping the CD8-binding site. The smaller interface probably represents the interaction between Ly49A on the NK cell and MHC-I on the target cell, whereas the larger one suggests an interaction between Ly49A and MHC-I on the NK cell itself. Both Ly49A binding sites on MHC-I are spatially distinct from that of the T-cell receptor.
- Subjects :
- Models, Molecular
Protein Folding
Glycosylation
Stereochemistry
Macromolecular Substances
Protein Conformation
Protein subunit
Molecular Sequence Data
Biology
Major histocompatibility complex
Crystallography, X-Ray
Natural killer cell
chemistry.chemical_compound
MHC class I
medicine
Escherichia coli
Antigens, Ly
Humans
Lectins, C-Type
Binding site
Receptors, Immunologic
Receptor
Histocompatibility Antigen H-2D
Multidisciplinary
H-2 Antigens
Ligand (biochemistry)
Recombinant Proteins
Cell biology
Killer Cells, Natural
medicine.anatomical_structure
chemistry
biology.protein
Sequence Alignment
Protein Binding
Receptors, NK Cell Lectin-Like
Signal Transduction
Subjects
Details
- ISSN :
- 00280836
- Volume :
- 402
- Issue :
- 6762
- Database :
- OpenAIRE
- Journal :
- Nature
- Accession number :
- edsair.doi.dedup.....89c418e24626fdf60a97a2ce6709aad7