KIR2DS4

KIR2DS4
Available structures
PDBHuman UniProt search: PDBe RCSB
Identifiers
AliasesKIR2DS4, CD158I, KIR1D, KIR2DS1, KIR412, KKA3, NKAT-8, NKAT8, KIR-2DS4, killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 4
External IDsOMIM: 604955; GeneCards: KIR2DS4; OMA:KIR2DS4 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_012314
NM_001281971
NM_001281972

n/a

RefSeq (protein)

NP_001268900
NP_001268901
NP_036446
NP_001268900.1

n/a

Location (UCSC)Chr 19: 54.83 – 54.85 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

Killer cell immunoglobulin-like receptor 2DS4 is a protein that in humans is encoded by the KIR2DS4 gene.[3][4][5]

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 (DAP12) 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.[5]

KIR2DS4 is a product of a gene conversion with KIR3DL2.[6] KIR2DS4 has unusual HLA-I specificity binding some HLA-C allotypes and HLA-A*11.[6] A common allele of KIR2DS4 encodes a truncated version (KIR-1D) that has no HLA-I binding ability.[6][7] Recent evidence suggests KIR2DS4 detects HLA-C presented peptides in a peptide-specific manner, detecting peptides conserved in bacteria.[8][9][10]

See also

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References

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  1. ^ a b c ENSG00000274406, ENSG00000277078, ENSG00000274807, ENSG00000275353, ENSG00000275731, ENSG00000273526, ENSG00000275351, ENSG00000274921, ENSG00000277345, ENSG00000276885, ENSG00000284408, ENSG00000274957, ENSG00000276154, ENSG00000284307, ENSG00000283779, ENSG00000274324, ENSG00000221957, ENSG00000274714, ENSG00000274533, ENSG00000276209, ENSG00000276634, ENSG00000276465, ENSG00000274947, ENSG00000283727, ENSG00000283846, ENSG00000276395, ENSG00000275938, ENSG00000284244, ENSG00000284264, ENSG00000283870, ENSG00000283882, ENSG00000276254 GRCh38: Ensembl release 89: ENSG00000273931, ENSG00000274406, ENSG00000277078, ENSG00000274807, ENSG00000275353, ENSG00000275731, ENSG00000273526, ENSG00000275351, ENSG00000274921, ENSG00000277345, ENSG00000276885, ENSG00000284408, ENSG00000274957, ENSG00000276154, ENSG00000284307, ENSG00000283779, ENSG00000274324, ENSG00000221957, ENSG00000274714, ENSG00000274533, ENSG00000276209, ENSG00000276634, ENSG00000276465, ENSG00000274947, ENSG00000283727, ENSG00000283846, ENSG00000276395, ENSG00000275938, ENSG00000284244, ENSG00000284264, ENSG00000283870, ENSG00000283882, ENSG00000276254Ensembl, May 2017
  2. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ^ Bottino C, Sivori S, Vitale M, Cantoni C, Falco M, Pende D, Morelli L, Augugliaro R, Semenzato G, Biassoni R, Moretta L, Moretta A (Oct 1996). "A novel surface molecule homologous to the p58/p50 family of receptors is selectively expressed on a subset of human natural killer cells and induces both triggering of cell functions and proliferation". Eur J Immunol. 26 (8): 1816–24. doi:10.1002/eji.1830260823. PMID 8765026. S2CID 23526107.
  4. ^ Wagtmann N, Biassoni R, Cantoni C, Verdiani S, Malnati MS, Vitale M, Bottino C, Moretta L, Moretta A, Long EO (Jun 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. doi:10.1016/1074-7613(95)90025-X. PMID 7749980.
  5. ^ a b "Entrez Gene: KIR2DS4 killer cell immunoglobulin-like receptor, two domains, short cytoplasmic tail, 4".
  6. ^ a b c Graef T, Moesta AK, Norman PJ, Abi-Rached L, Vago L, Older Aguilar AM, Gleimer M, Hammond JA, Guethlein LA, Bushnell DA, Robinson PJ, Parham P (2009-10-26). "KIR2DS4 is a product of gene conversion with KIR3DL2 that introduced specificity for HLA-A*11 while diminishing avidity for HLA-C". Journal of Experimental Medicine. 206 (11): 2557–2572. doi:10.1084/jem.20091010. ISSN 1540-9538. PMC 2768862. PMID 19858347.
  7. ^ Middleton D, Gonzalez A, Gilmore PM (February 2007). "Studies on the Expression of the Deleted KIR2DS4*003 Gene Product and Distribution of KIR2DS4 Deleted and Nondeleted Versions in Different Populations". Human Immunology. 68 (2): 128–134. doi:10.1016/j.humimm.2006.12.007. PMID 17321903.
  8. ^ Sim MJ, Rajagopalan S, Altmann DM, Boyton RJ, Sun PD, Long EO (2019-06-25). "Human NK cell receptor KIR2DS4 detects a conserved bacterial epitope presented by HLA-C". Proceedings of the National Academy of Sciences. 116 (26): 12964–12973. doi:10.1073/pnas.1903781116. ISSN 0027-8424. PMC 6601252. PMID 31138701.
  9. ^ Parham P (2019-06-25). "A natural killer cell receptor takes sharp aim at the world of bacteria". Proceedings of the National Academy of Sciences. 116 (26): 12601–12603. doi:10.1073/pnas.1907937116. ISSN 0027-8424. PMC 6601266. PMID 31175150.
  10. ^ Sim MJ, Brennan P, Wahl KL, Lu J, Rajagopalan S, Sun PD, Long EO (2023-09-29). "Innate receptors with high specificity for HLA class I–peptide complexes". Science Immunology. 8 (87): eadh1781. doi:10.1126/sciimmunol.adh1781. ISSN 2470-9468. PMID 37683038.

Further reading

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This article incorporates text from the United States National Library of Medicine, which is in the public domain.