HCSGD entry for KLRK1
1. General information
Official gene symbol | KLRK1 |
---|---|
Entrez ID | 22914 |
Gene full name | killer cell lectin-like receptor subfamily K, member 1 |
Other gene symbols | CD314 D12S2489E KLR NKG2-D NKG2D |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0002223 | Stimulatory C-type lectin receptor signaling pathway | IEA | biological_process |
GO:0004872 | Receptor activity | TAS | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005886 | Plasma membrane | TAS | cellular_component |
GO:0005887 | Integral component of plasma membrane | TAS | cellular_component |
GO:0007165 | Signal transduction | TAS | biological_process |
GO:0009897 | External side of plasma membrane | IEA | cellular_component |
GO:0009986 | Cell surface | IDA | cellular_component |
GO:0016021 | Integral component of membrane | TAS | cellular_component |
GO:0030101 | Natural killer cell activation | IEA TAS | biological_process |
GO:0030246 | Carbohydrate binding | IEA | molecular_function |
GO:0031295 | T cell costimulation | TAS | biological_process |
GO:0032394 | MHC class Ib receptor activity | IEA | molecular_function |
GO:0032729 | Positive regulation of interferon-gamma production | IEA | biological_process |
GO:0042288 | MHC class I protein binding | IEA | molecular_function |
GO:0042803 | Protein homodimerization activity | IEA | molecular_function |
GO:0045087 | Innate immune response | TAS | biological_process |
GO:0045429 | Positive regulation of nitric oxide biosynthetic process | IEA | biological_process |
GO:0045954 | Positive regulation of natural killer cell mediated cytotoxicity | IEA | biological_process |
GO:0050776 | Regulation of immune response | TAS | biological_process |
GO:0050830 | Defense response to Gram-positive bacterium | IEA | biological_process |
GO:0071222 | Cellular response to lipopolysaccharide | IEA | biological_process |
Entries Per Page
Displaying Page of
4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.9820557236 | 0.5187597508 | 0.9999902473 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log 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 | - | - |
GSE48662 | Down | -0.0618472999 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-335-5p | MIMAT0000765 | MIRT017175 | Microarray | Functional MTI (Weak) | 18185580 |
hsa-miR-148b-3p | MIMAT0000759 | MIRT019249 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-9-5p | MIMAT0000441 | MIRT021363 | Microarray | Functional MTI (Weak) | 17612493 |
Entries Per Page
Displaying Page of
- mirRecord
No target information from mirRecord
- 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 |
---|---|
27853638 | Melphalan 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 |
26878797 | Here 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 |
26878797 | The 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 |
26878797 | In liver fibrosis, the accumulation of senescent activated stellate cells is increased in mice lacking NKG2D receptor leading to increased fibrosis |
26878797 | Overall, 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 |
26474283 | On the other hand, axitinib, through the DDR induction, is also able to increase the surface NKG2D ligand expression |
24913980 | In this article, we identify the signaling events underlying chemotherapy-induced NKG2D and DNAM-1 ligand expression on multiple myeloma (MM) cells |
24043758 | The elimination of senescent tumor cells is dependent on NKG2D |
24043758 | Our 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 |
21764762 | Human NK cells are alerted to induction of p53 in cancer cells by upregulation of the NKG2D ligands ULBP1 and ULBP2 |
21764762 | Natural 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 |
21764762 | For example, induction of DNA damage or cellular senescence pathways in tumor cells led to upregulation of NKG2D ligands that activate NK cells |
21764762 | Although, both pathways activate p53, the relationship of p53 activation to upregulation of NKG2D ligands has not been addressed |
21764762 | Taken together, our findings define the involvement of p53 in the regulation of specific NKG2D ligands that enhance NK cell-mediated target recognition |
19098271 | ATM-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 |
19098271 | Induction 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 |
19098271 | In 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 |
19098271 | Accordingly, therapeutic drug treatment of MM cells increases NK-cell degranulation, the NKG2D and DNAM-1 receptors being the major triggering molecules |
19098271 | Drug-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 |
16461801 | Such 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 |
Entries Per Page
Displaying Page of