Open Access Articles- Top Results for KLRC2


SymbolsKLRC2 ; CD159c; NKG2-C; NKG2C
External IDsOMIM602891 HomoloGene135919 GeneCards: KLRC2 Gene
RNA expression pattern
File:PBB GE KLRC2 206785 s at tn.png
More reference expression data
RefSeq (mRNA)NM_002260n/a
RefSeq (protein)NP_002251n/a
Location (UCSC)Chr 12:
10.58 – 10.59 Mb
PubMed search[1]n/a

NKG2-C type II integral membrane protein is a protein that in humans is encoded by the KLRC2 gene.[1][2]


Natural killer (NK) cells are lymphocytes that can mediate lysis of certain tumor cells and virus-infected cells without previous activation. They can also regulate specific humoral and cell-mediated immunity. NK cells preferentially express several calcium-dependent (C-type) lectins, which have been implicated in the regulation of NK cell function. The group, designated KLRC (NKG2) are expressed primarily in natural killer (NK) cells and encodes a family of transmembrane proteins characterized by a type II membrane orientation (extracellular C terminus) and the presence of a C-type lectin domain. The KLRC (NKG2) gene family is located within the NK complex, a region that contains several C-type lectin genes preferentially expressed on NK cells. KLRC2 alternative splice variants have been described but their full-length nature has not been determined.[2]


KLRC2 has been shown to interact with KLRD1.[3][4] The binding of this CD94/NKG2C heterodimer to its cellular ligand HLA-E has been shown to drive the expansion of a subset of Natural Killer (NK) cells in response to viral infections.[5]

See also


  1. ^ Plougastel B, Trowsdale J (Apr 1998). "Sequence analysis of a 62-kb region overlapping the human KLRC cluster of genes". Genomics 49 (2): 193–9. PMID 9598306. doi:10.1006/geno.1997.5197. 
  2. ^ a b "Entrez Gene: KLRC2 killer cell lectin-like receptor subfamily C, member 2". 
  3. ^ Lazetic S, Chang C, Houchins JP, Lanier LL, Phillips JH (Dec 1996). "Human natural killer cell receptors involved in MHC class I recognition are disulfide-linked heterodimers of CD94 and NKG2 subunits". Journal of Immunology 157 (11): 4741–5. PMID 8943374. 
  4. ^ Ding Y, Sumitran S, Holgersson J (May 1999). "Direct binding of purified HLA class I antigens by soluble NKG2/CD94 C-type lectins from natural killer cells". Scandinavian Journal of Immunology 49 (5): 459–65. PMID 10320637. doi:10.1046/j.1365-3083.1999.00566.x. 
  5. ^ Rölle A, Pollmann J, Ewen EM, Le VT, Halenius A, Hengel H et al. (Dec 2014). "IL-12-producing monocytes and HLA-E control HCMV-driven NKG2C+ NK cell expansion". The Journal of Clinical Investigation 124 (12): 5305-16. PMID 25384219. doi:10.1172/JCI77440. 

Further reading

  • Houchins JP, Yabe T, McSherry C, Bach FH (Apr 1991). "DNA sequence analysis of NKG2, a family of related cDNA clones encoding type II integral membrane proteins on human natural killer cells". The Journal of Experimental Medicine 173 (4): 1017–20. PMC 2190798. PMID 2007850. doi:10.1084/jem.173.4.1017. 
  • Yabe T, McSherry C, Bach FH, Fisch P, Schall RP, Sondel PM et al. (1993). "A multigene family on human chromosome 12 encodes natural killer-cell lectins". Immunogenetics 37 (6): 455–60. PMID 8436421. doi:10.1007/BF00222470. 
  • Houchins JP, Lanier LL, Niemi EC, Phillips JH, Ryan JC (Apr 1997). "Natural killer cell cytolytic activity is inhibited by NKG2-A and activated by NKG2-C". Journal of Immunology 158 (8): 3603–9. PMID 9103421. 
  • Braud VM, Allan DS, O'Callaghan CA, Söderström K, D'Andrea A, Ogg GS et al. (Feb 1998). "HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C". Nature 391 (6669): 795–9. PMID 9486650. doi:10.1038/35869. 
  • Lanier LL, Corliss B, Wu J, Phillips JH (Jun 1998). "Association of DAP12 with activating CD94/NKG2C NK cell receptors". Immunity 8 (6): 693–701. PMID 9655483. doi:10.1016/S1074-7613(00)80574-9. 
  • Glienke J, Sobanov Y, Brostjan C, Steffens C, Nguyen C, Lehrach H et al. (Aug 1998). "The genomic organization of NKG2C, E, F, and D receptor genes in the human natural killer gene complex". Immunogenetics 48 (3): 163–73. PMID 9683661. doi:10.1007/s002510050420. 
  • Ding Y, Sumitran S, Holgersson J (May 1999). "Direct binding of purified HLA class I antigens by soluble NKG2/CD94 C-type lectins from natural killer cells". Scandinavian Journal of Immunology 49 (5): 459–65. PMID 10320637. doi:10.1046/j.1365-3083.1999.00566.x. 
  • Khakoo SI, Rajalingam R, Shum BP, Weidenbach K, Flodin L, Muir DG et al. (Jun 2000). "Rapid evolution of NK cell receptor systems demonstrated by comparison of chimpanzees and humans". Immunity 12 (6): 687–98. PMID 10894168. doi:10.1016/S1074-7613(00)80219-8. 
  • Shum BP, Flodin LR, Muir DG, Rajalingam R, Khakoo SI, Cleland S et al. (Jan 2002). "Conservation and variation in human and common chimpanzee CD94 and NKG2 genes". Journal of Immunology 168 (1): 240–52. PMID 11751968. doi:10.4049/jimmunol.168.1.240. 
  • Hikami K, Tsuchiya N, Yabe T, Tokunaga K (Mar 2003). "Variations of human killer cell lectin-like receptors: common occurrence of NKG2-C deletion in the general population". Genes and Immunity 4 (2): 160–7. PMID 12618865. doi:10.1038/sj.gene.6363940. 
  • Miyashita R, Tsuchiya N, Hikami K, Kuroki K, Fukazawa T, Bijl M et al. (Jan 2004). "Molecular genetic analyses of human NKG2C (KLRC2) gene deletion". International Immunology 16 (1): 163–8. PMID 14688071. doi:10.1093/intimm/dxh013. 
  • Ortega C, Romero P, Palma A, Orta T, Peña J, García-Vinuesa A et al. (Dec 2004). "Role for NKG2-A and NKG2-C surface receptors in chronic CD4+ T-cell responses". Immunology and Cell Biology 82 (6): 587–95. PMID 15550116. doi:10.1111/j.0818-9641.2004.01284.x. 
  • Gumá M, Busch LK, Salazar-Fontana LI, Bellosillo B, Morte C, García P et al. (Jul 2005). "The CD94/NKG2C killer lectin-like receptor constitutes an alternative activation pathway for a subset of CD8+ T cells". European Journal of Immunology 35 (7): 2071–80. PMID 15940674. doi:10.1002/eji.200425843. 

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

Lua error in package.lua at line 80: module 'Module:Buffer' not found.