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KIR3DL1

KIR3DL1
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesKIR3DL1, CD158E1, KIR, KIR3DL1/S1, NKAT-3, NKAT3, NKB1, NKB1B, KIR3DL2, killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 1, KIR2DL5B
External IDsOMIM: 604946; MGI: 3612791; HomoloGene: 135918; GeneCards: KIR3DL1; OMA:KIR3DL1 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_013289
NM_001322168

NM_177748

RefSeq (protein)

NP_001309097
NP_037421

NP_808416

Location (UCSC)Chr 19: 54.82 – 54.83 MbChr X: 135.35 – 135.44 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Killer cell immunoglobulin-like receptor 3DL1 is a protein that in humans is encoded by the KIR3DL1 gene.[5][6][7]

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 immunoglobulin-like 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.[7]

See also

References

  1. ^ a b c ENSG00000274146, ENSG00000278368, ENSG00000273775, ENSG00000276501, ENSG00000278427, ENSG00000274948, ENSG00000274036, ENSG00000274920, ENSG00000275786, ENSG00000276329, ENSG00000277272, ENSG00000283954, ENSG00000275486, ENSG00000275545, ENSG00000278079, ENSG00000273518, ENSG00000275717, ENSG00000277175, ENSG00000167633, ENSG00000283729, ENSG00000283731, ENSG00000276423, ENSG00000275659, ENSG00000278856, ENSG00000284426, ENSG00000275288, ENSG00000284093, ENSG00000283827, ENSG00000284177, ENSG00000276379, ENSG00000284342 GRCh38: Ensembl release 89: ENSG00000284589, ENSG00000274146, ENSG00000278368, ENSG00000273775, ENSG00000276501, ENSG00000278427, ENSG00000274948, ENSG00000274036, ENSG00000274920, ENSG00000275786, ENSG00000276329, ENSG00000277272, ENSG00000283954, ENSG00000275486, ENSG00000275545, ENSG00000278079, ENSG00000273518, ENSG00000275717, ENSG00000277175, ENSG00000167633, ENSG00000283729, ENSG00000283731, ENSG00000276423, ENSG00000275659, ENSG00000278856, ENSG00000284426, ENSG00000275288, ENSG00000284093, ENSG00000283827, ENSG00000284177, ENSG00000276379, ENSG00000284342Ensembl, 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. ^ Colonna M, Samaridis J (May 1995). "Cloning of immunoglobulin-superfamily members associated with HLA-C and HLA-B recognition by human natural killer cells". Science. 268 (5209): 405–8. Bibcode:1995Sci...268..405C. doi:10.1126/science.7716543. PMID 7716543.
  6. ^ 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.
  7. ^ a b "Entrez Gene: KIR3DL1 killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail, 1".

Further reading

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


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