KLRK1

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 NKG2 gene family is located within the NK complex, a region that contains several C-type lectin genes preferentially expressed in NK cells. This gene encodes a member of the NKG2 family. The encoded transmembrane protein is characterized by a type II membrane orientation (has an extracellular C terminus) and the presence of a C-type lectin domain. It binds to a diverse family of ligands that include MHC class I chain-related A and B proteins and UL-16 binding proteins, where ligand-receptor interactions can result in the activation of NK and T cells. The surface expression of these ligands is important for the recognition of stressed cells by the immune system, and thus this protein and its ligands are therapeutic targets for the treatment of immune diseases and cancers. Read-through transcription exists between this gene and the upstream KLRC4 (killer cell lectin-like receptor subfamily C, member 4) family member in the same cluster. [provided by RefSeq, Dec 2010]

Full Name

Killer Cell Lectin Like Receptor K1

Function

Functions as an activating and costimulatory receptor involved in immunosurveillance upon binding to various cellular stress-inducible ligands displayed at the surface of autologous tumor cells and virus-infected cells. Provides both stimulatory and costimulatory innate immune responses on activated killer (NK) cells, leading to cytotoxic activity. Acts as a costimulatory receptor for T-cell receptor (TCR) in CD8(+) T-cell-mediated adaptive immune responses by amplifying T-cell activation. Stimulates perforin-mediated elimination of ligand-expressing tumor cells. Signaling involves calcium influx, culminating in the expression of TNF-alpha. Participates in NK cell-mediated bone marrow graft rejection. May play a regulatory role in differentiation and survival of NK cells. Binds to ligands belonging to various subfamilies of MHC class I-related glycoproteins including MICA, MICB, RAET1E, RAET1G, RAET1L/ULBP6, ULBP1, ULBP2, ULBP3 (ULBP2>ULBP1>ULBP3) and ULBP4.

Biological Process

Adaptive immune responseIEA:UniProtKB-KW
Cell differentiationIEA:UniProtKB-KW
Cellular response to lipopolysaccharideIEA:Ensembl
Defense response to Gram-positive bacteriumIEA:Ensembl
Natural killer cell activationManual Assertion Based On ExperimentTAS:BHF-UCL
Natural killer cell mediated cytotoxicityManual Assertion Based On ExperimentIDA:UniProtKB
Negative regulation of GTPase activityManual Assertion Based On ExperimentIDA:CACAO
Negative regulation of natural killer cell chemotaxisManual Assertion Based On ExperimentIDA:CACAO
Positive regulation of interferon-gamma productionIEA:Ensembl
Positive regulation of natural killer cell mediated cytotoxicityManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of nitric oxide biosynthetic processIEA:Ensembl
Signal transductionManual Assertion Based On ExperimentTAS:ProtInc
Stimulatory C-type lectin receptor signaling pathwayIEA:Ensembl
T cell costimulationManual Assertion Based On ExperimentTAS:BHF-UCL

Cellular Location

Cell membrane
Colocalized with HCST on the cell surface.

Topology

Cytoplasmic: 1-51
Helical: 52-72
Extracellular: 73-216

Anti-KLRK1 antibodies

Fig.3 Signaling pathways in cancers. (Creative Biolabs Authorized)