KLRB1

Killer cell lectin-like receptor subfamily B, member 1, also known as KLRB1, NKR-P1A or CD161 (cluster of differentiation 161), is a human gene.[5]

KLRB1
Identifiers
AliasesKLRB1, CD161, CLEC5B, NKR, NKR-P1, NKR-P1A, NKRP1A, hNKR-P1A, killer cell lectin like receptor B1
External IDsOMIM: 602890 MGI: 107540 HomoloGene: 84369 GeneCards: KLRB1
Gene location (Human)
Chr.Chromosome 12 (human)[1]
Band12p13.31Start9,594,551 bp[1]
End9,607,916 bp[1]
RNA expression pattern
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez

3820

17057

Ensembl

ENSG00000111796

ENSMUSG00000030361

UniProt

Q12918

P27811

RefSeq (mRNA)

NM_002258

NM_001159902
NM_010737

RefSeq (protein)

NP_002249

NP_001153374
NP_034867

Location (UCSC)Chr 12: 9.59 – 9.61 MbChr 6: 128.61 – 128.62 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

Natural killer (NK) cells are lymphocytes that mediate cytotoxicity and secrete cytokines after immune stimulation. Several genes of the C-type lectin superfamily, including the rodent NKRP1 family of glycoproteins, are expressed by NK cells and may be involved in the regulation of NK cell function. The KLRB1 protein contains an extracellular domain with several motifs characteristic of C-type lectins, a transmembrane domain, and a cytoplasmic domain. The KLRB1 protein, NKR-P1A or CD161, is classified as a type II membrane protein because it has an external C terminus.[5] NKR-P1A, the receptor encoded by the KLRB1 gene, recognizes Lectin Like Transcript-1 (LLT1) as a functional ligand.

References

  1. GRCh38: Ensembl release 89: ENSG00000111796 - Ensembl, May 2017
  2. GRCm38: Ensembl release 89: ENSMUSG00000030361 - Ensembl, 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. "Entrez Gene: KLRB1 killer cell lectin-like receptor subfamily B, member 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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