HCSGD entry for KLRK1


1. General information

Official gene symbolKLRK1
Entrez ID22914
Gene full namekiller cell lectin-like receptor subfamily K, member 1
Other gene symbolsCD314 D12S2489E KLR NKG2-D NKG2D
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0002223Stimulatory C-type lectin receptor signaling pathwayIEAbiological_process
GO:0004872Receptor activityTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005886Plasma membraneTAScellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0007165Signal transductionTASbiological_process
GO:0009897External side of plasma membraneIEAcellular_component
GO:0009986Cell surfaceIDAcellular_component
GO:0016021Integral component of membraneTAScellular_component
GO:0030101Natural killer cell activationIEA TASbiological_process
GO:0030246Carbohydrate bindingIEAmolecular_function
GO:0031295T cell costimulationTASbiological_process
GO:0032394MHC class Ib receptor activityIEAmolecular_function
GO:0032729Positive regulation of interferon-gamma productionIEAbiological_process
GO:0042288MHC class I protein bindingIEAmolecular_function
GO:0042803Protein homodimerization activityIEAmolecular_function
GO:0045087Innate immune responseTASbiological_process
GO:0045429Positive regulation of nitric oxide biosynthetic processIEAbiological_process
GO:0045954Positive regulation of natural killer cell mediated cytotoxicityIEAbiological_process
GO:0050776Regulation of immune responseTASbiological_process
GO:0050830Defense response to Gram-positive bacteriumIEAbiological_process
GO:0071222Cellular response to lipopolysaccharideIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.98205572360.51875975080.99999024731.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954--
GSE13712_SHEAR--
GSE13712_STATIC--
GSE19018--
GSE19899_A1--
GSE19899_A2--
PubMed_21979375_A1--
PubMed_21979375_A2--
GSE35957--
GSE36640--
GSE54402--
GSE9593--
GSE43922--
GSE24585--
GSE37065--
GSE28863_A1--
GSE28863_A2--
GSE28863_A3--
GSE28863_A4--
GSE48662Down-0.0618472999

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-335-5pMIMAT0000765MIRT017175MicroarrayFunctional MTI (Weak)18185580
hsa-miR-148b-3pMIMAT0000759MIRT019249MicroarrayFunctional MTI (Weak)17612493
hsa-miR-9-5pMIMAT0000441MIRT021363MicroarrayFunctional MTI (Weak)17612493
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    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 8 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27853638Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells
26878797Here we show that ligands of an activating Natural Killer (NK) cell receptor (NKG2D), MICA and ULBP2 are consistently up-regulated following induction of replicative senescence, oncogene-induced senescence and DNA damage - induced senescence
26878797The mechanisms regulating the initial expression of NKG2D ligands in senescent cells are dependent on a DNA damage response, whilst continuous expression of these ligands is regulated by the ERK signaling pathway
26878797In liver fibrosis, the accumulation of senescent activated stellate cells is increased in mice lacking NKG2D receptor leading to increased fibrosis
26878797Overall, our results provide new insights into the mechanisms regulating the expression of immune ligands in senescent cells and reveal the importance of NKG2D receptor-ligand interaction in protecting against liver fibrosis
26474283On the other hand, axitinib, through the DDR induction, is also able to increase the surface NKG2D ligand expression
24913980In this article, we identify the signaling events underlying chemotherapy-induced NKG2D and DNAM-1 ligand expression on multiple myeloma (MM) cells
24043758The elimination of senescent tumor cells is dependent on NKG2D
24043758Our findings suggest that elimination of senescent tumors by NK cells occurs as a result of the cooperation of signals associated with p53 expression or senescence, which regulate NK cell recruitment, and other signals that induce NKG2D ligand expression on tumor cells
21764762Human NK cells are alerted to induction of p53 in cancer cells by upregulation of the NKG2D ligands ULBP1 and ULBP2
21764762Natural killer (NK) cells are immune cells sensing and eliminating foreign, stressed, transformed, and senescent cells through specialized surface receptors, such as NKG2D, that interacts with several virus- or stress-inducible ligands, including ULBP1 and -2, which are expressed on target cell surfaces
21764762For example, induction of DNA damage or cellular senescence pathways in tumor cells led to upregulation of NKG2D ligands that activate NK cells
21764762Although, both pathways activate p53, the relationship of p53 activation to upregulation of NKG2D ligands has not been addressed
21764762Taken together, our findings define the involvement of p53 in the regulation of specific NKG2D ligands that enhance NK cell-mediated target recognition
19098271ATM-ATR-dependent up-regulation of DNAM-1 and NKG2D ligands on multiple myeloma cells by therapeutic agents results in enhanced NK-cell susceptibility and is associated with a senescent phenotype
19098271Induction of DNA damage response has been recently shown capable of enhancing NKG2D ligand (NKG2DL) expression, but nothing is known about DNAM-1 ligand (DNAM-1L) regulation
19098271In this study, we show that myeloma cells treated with low doses of therapeutic agents commonly used in the management of patients with MM, such as doxorubicin, melphalan, and bortezomib, up-regulate DNAM-1 and NKG2D ligands
19098271Accordingly, therapeutic drug treatment of MM cells increases NK-cell degranulation, the NKG2D and DNAM-1 receptors being the major triggering molecules
19098271Drug-induced DNAM-1 and NKG2D ligand expression was abolished after treatment with the ATM (ataxia telangiectasia mutated) and ATR (ATM- and RAD3-related) pharmacologic inhibitors caffeine and KU-55933, and was preferentially associated with senescent cells arrested in the G2 phase of the cell cycle
16461801Such regulatory receptors include stimulatory and inhibitory members of the killer immunoglobulin-like receptor (KIR) family, the stimulatory c-type lectin receptor NKG2D, and CX3CR1, the receptor for the chemokine fractalkine
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