Killer cell immunoglobulin-like receptor 3DL3 is a protein that in humans is encoded by the KIR3DL3 gene.[5][6]

KIR3DL3
Identifiers
AliasesKIR3DL3, CD158Z, KIR3DL7, KIR44, KIRC1, KIR2DS2, killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 3
External IDsOMIM: 610095; MGI: 3612791; HomoloGene: 77448; GeneCards: KIR3DL3; OMA:KIR3DL3 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_153443

NM_177748

RefSeq (protein)

NP_703144

NP_808416

Location (UCSC)Chr 19: 54.72 – 54.74 MbChr X: 135.35 – 135.44 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

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, KIR2DL4, 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.[6]

References

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  1. ^ a b c ENSG00000283823, ENSG00000274511, ENSG00000276196, ENSG00000275433, ENSG00000276086, ENSG00000283875, ENSG00000274480, ENSG00000277392, ENSG00000274786, ENSG00000274724, ENSG00000276930, ENSG00000276572, ENSG00000284371, ENSG00000276084, ENSG00000284104, ENSG00000278729, ENSG00000277028, ENSG00000275062, ENSG00000274763, ENSG00000276433, ENSG00000274639, ENSG00000283966, ENSG00000284127, ENSG00000277552, ENSG00000278490, ENSG00000276806, ENSG00000242019, ENSG00000276328, ENSG00000276875, ENSG00000274556, ENSG00000283915, ENSG00000284086, ENSG00000278723, ENSG00000284480, ENSG00000273502, ENSG00000274254, ENSG00000275172, ENSG00000275513, ENSG00000277620, ENSG00000274696, ENSG00000277596 GRCh38: Ensembl release 89: ENSG00000274394, ENSG00000283823, ENSG00000274511, ENSG00000276196, ENSG00000275433, ENSG00000276086, ENSG00000283875, ENSG00000274480, ENSG00000277392, ENSG00000274786, ENSG00000274724, ENSG00000276930, ENSG00000276572, ENSG00000284371, ENSG00000276084, ENSG00000284104, ENSG00000278729, ENSG00000277028, ENSG00000275062, ENSG00000274763, ENSG00000276433, ENSG00000274639, ENSG00000283966, ENSG00000284127, ENSG00000277552, ENSG00000278490, ENSG00000276806, ENSG00000242019, ENSG00000276328, ENSG00000276875, ENSG00000274556, ENSG00000283915, ENSG00000284086, ENSG00000278723, ENSG00000284480, ENSG00000273502, ENSG00000274254, ENSG00000275172, ENSG00000275513, ENSG00000277620, ENSG00000274696, ENSG00000277596Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000057439Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Long EO, Barber DF, Burshtyn DN, Faure M, Peterson M, Rajagopalan S, Renard V, Sandusky M, Stebbins CC, Wagtmann N, Watzl C (Aug 2001). "Inhibition of natural killer cell activation signals by killer cell immunoglobulin-like receptors (CD158)". Immunol Rev. 181: 223–233. doi:10.1034/j.1600-065X.2001.1810119.x. PMID 11513144. S2CID 13312691.
  6. ^ a b "Entrez Gene: KIR3DL3 killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail, 3".

Further reading

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