KIR3DL1
From Wikipedia, the free encyclopedia
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Killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail, 1
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| Symbol(s) | KIR3DL1; KIR; AMB11; CD158E1; CD158E1/2; CD158E2; CL-11; CL-2; KIR-G1; KIR3DL1/2V; KIR3DS1; MGC119726; MGC119728; MGC126589; MGC126591; NKAT10; NKAT3; NKB1; NKB1B | |||||||||||||
| External IDs | OMIM: 604946 MGI: 3612791 HomoloGene: 77448 | |||||||||||||
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| RNA expression pattern | ||||||||||||||
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| Orthologs | ||||||||||||||
| Human | Mouse | |||||||||||||
| Entrez | 3811 | 245615 | ||||||||||||
| Ensembl | ENSG00000167633 | ENSMUSG00000057439 | ||||||||||||
| Uniprot | P43629 | Q673W3 | ||||||||||||
| Refseq | NM_013289 (mRNA) NP_037421 (protein) |
NM_177748 (mRNA) NP_808416 (protein) |
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| Location | Chr 19: 60.02 - 60.03 Mb | Chr X: 131.8 - 131.82 Mb | ||||||||||||
| Pubmed search | [1] | [2] | ||||||||||||
Killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail, 1, also known as KIR3DL1, is a human gene.[1]
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.[1]
[edit] See also
[edit] References
[edit] Further reading
- Selvakumar A, Steffens U, Dupont B (1997). "Polymorphism and domain variability of human killer cell inhibitory receptors.". Immunol. Rev. 155: 183-96. PMID 9059894.
- D'Andrea A, Chang C, Franz-Bacon K, et al. (1995). "Molecular cloning of NKB1. A natural killer cell receptor for HLA-B allotypes.". J. Immunol. 155 (5): 2306-10. PMID 7650366.
- Colonna M, Samaridis J (1995). "Cloning of immunoglobulin-superfamily members associated with HLA-C and HLA-B recognition by human natural killer cells.". Science 268 (5209): 405-8. PMID 7716543.
- Wagtmann N, Biassoni R, Cantoni C, et al. (1995). "Molecular clones of the p58 NK cell receptor reveal immunoglobulin-related molecules with diversity in both the extra- and intracellular domains.". Immunity 2 (5): 439-49. PMID 7749980.
- Litwin V, Gumperz J, Parham P, et al. (1994). "NKB1: a natural killer cell receptor involved in the recognition of polymorphic HLA-B molecules.". J. Exp. Med. 180 (2): 537-43. PMID 8046332.
- Döhring C, Samaridis J, Colonna M (1996). "Alternatively spliced forms of human killer inhibitory receptors.". Immunogenetics 44 (3): 227-30. PMID 8662091.
- Pende D, Biassoni R, Cantoni C, et al. (1996). "The natural killer cell receptor specific for HLA-A allotypes: a novel member of the p58/p70 family of inhibitory receptors that is characterized by three immunoglobulin-like domains and is expressed as a 140-kD disulphide-linked dimer.". J. Exp. Med. 184 (2): 505-18. PMID 8760804.
- Wagtmann N, Rajagopalan S, Winter CC, et al. (1996). "Killer cell inhibitory receptors specific for HLA-C and HLA-B identified by direct binding and by functional transfer.". Immunity 3 (6): 801-9. PMID 8777725.
- Valiante NM, Uhrberg M, Shilling HG, et al. (1998). "Functionally and structurally distinct NK cell receptor repertoires in the peripheral blood of two human donors.". Immunity 7 (6): 739-51. PMID 9430220.
- Uhrberg M, Valiante NM, Shum BP, et al. (1998). "Human diversity in killer cell inhibitory receptor genes.". Immunity 7 (6): 753-63. PMID 9430221.
- Vyas Y, Selvakumar A, Steffens U, Dupont B (1999). "Multiple transcripts of the killer cell immunoglobulin-like receptor family, KIR3DL1 (NKB1), are expressed by natural killer cells of a single individual.". Tissue Antigens 52 (6): 510-9. PMID 9894849.
- Kwon D, Chwae YJ, Choi IH, et al. (2000). "Diversity of the p70 killer cell inhibitory receptor (KIR3DL) family members in a single individual.". Mol. Cells 10 (1): 54-60. PMID 10774747.
- Crum KA, Logue SE, Curran MD, Middleton D (2001). "Development of a PCR-SSOP approach capable of defining the natural killer cell inhibitory receptor (KIR) gene sequence repertoires.". Tissue Antigens 56 (4): 313-26. PMID 11098931.
- Gardiner CM, Guethlein LA, Shilling HG, et al. (2001). "Different NK cell surface phenotypes defined by the DX9 antibody are due to KIR3DL1 gene polymorphism.". J. Immunol. 166 (5): 2992-3001. PMID 11207248.
- Yamochi T, Semba K, Tsuji K, et al. (2002). "ik3-1/Cables is a substrate for cyclin-dependent kinase 3 (cdk 3).". Eur. J. Biochem. 268 (23): 6076-82. PMID 11733001.
- Shilling HG, Guethlein LA, Cheng NW, et al. (2002). "Allelic polymorphism synergizes with variable gene content to individualize human KIR genotype.". J. Immunol. 168 (5): 2307-15. PMID 11859120.
- Martin MP, Gao X, Lee JH, et al. (2002). "Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS.". Nat. Genet. 31 (4): 429-34. doi:. PMID 12134147.
- Chwae YJ, Chang MJ, Park SM, et al. (2002). "Molecular mechanism of the activation-induced cell death inhibition mediated by a p70 inhibitory killer cell Ig-like receptor in Jurkat T cells.". J. Immunol. 169 (7): 3726-35. PMID 12244166.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899-903. doi:. PMID 12477932.
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This article incorporates text from the United States National Library of Medicine, which is in the public domain.
