Cannabis Indica

KIR3DL2
Identifiers
AliasesKIR3DL2, CD158K, NKAT-4, NKAT4, NKAT4B, p140, 3DL2, KIR-3DL2, killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 2
External IDsOMIM: 604947 HomoloGene: 129622 GeneCards: KIR3DL2
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001242867
NM_006737

n/a

RefSeq (protein)

NP_001229796
NP_006728
NP_001229796.1

n/a

Location (UCSC)Chr 19: 54.85 – 54.87 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

Killer cell immunoglobulin-like receptor 3DL2 is a protein that in humans is encoded by the KIR3DL2 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 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.[5]

See also[edit]

References[edit]

  1. ^ a b c ENSG00000275838, ENSG00000277709, ENSG00000273735, ENSG00000284192, ENSG00000276004, ENSG00000278361, ENSG00000284046, ENSG00000278442, ENSG00000275416, ENSG00000275626, ENSG00000284295, ENSG00000278707, ENSG00000278758, ENSG00000278656, ENSG00000278850, ENSG00000284213, ENSG00000276424, ENSG00000284528, ENSG00000277982, ENSG00000274722, ENSG00000278726, ENSG00000275511, ENSG00000275083, ENSG00000273911, ENSG00000283975, ENSG00000276357, ENSG00000278809, ENSG00000277181, ENSG00000284384, ENSG00000283951, ENSG00000278403, ENSG00000275262, ENSG00000278710, ENSG00000275566, ENSG00000284063, ENSG00000276882, ENSG00000240403, ENSG00000276739, ENSG00000284466, ENSG00000278474, ENSG00000284381, ENSG00000288389 GRCh38: Ensembl release 89: ENSG00000275629, ENSG00000275838, ENSG00000277709, ENSG00000273735, ENSG00000284192, ENSG00000276004, ENSG00000278361, ENSG00000284046, ENSG00000278442, ENSG00000275416, ENSG00000275626, ENSG00000284295, ENSG00000278707, ENSG00000278758, ENSG00000278656, ENSG00000278850, ENSG00000284213, ENSG00000276424, ENSG00000284528, ENSG00000277982, ENSG00000274722, ENSG00000278726, ENSG00000275511, ENSG00000275083, ENSG00000273911, ENSG00000283975, ENSG00000276357, ENSG00000278809, ENSG00000277181, ENSG00000284384, ENSG00000283951, ENSG00000278403, ENSG00000275262, ENSG00000278710, ENSG00000275566, ENSG00000284063, ENSG00000276882, ENSG00000240403, ENSG00000276739, ENSG00000284466, ENSG00000278474, ENSG00000284381, ENSG00000288389Ensembl, May 2017
  2. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ^ 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.
  4. ^ Dohring C, Samaridis J, Colonna M (Aug 1996). "Alternatively spliced forms of human killer inhibitory receptors". Immunogenetics. 44 (3): 227–30. doi:10.1007/BF02602590. PMID 8662091. S2CID 38478576.
  5. ^ a b "Entrez Gene: KIR3DL2 killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail, 2".

Further reading[edit]

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


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