HCSGD entry for PRKDC
1. General information
Official gene symbol | PRKDC |
---|---|
Entrez ID | 5591 |
Gene full name | protein kinase, DNA-activated, catalytic polypeptide |
Other gene symbols | DNA-PKcs DNAPK DNPK1 HYRC HYRC1 XRCC7 p350 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0000723 | Telomere maintenance | IEA | biological_process |
GO:0001756 | Somitogenesis | IEA | biological_process |
GO:0002326 | B cell lineage commitment | IEA | biological_process |
GO:0002328 | Pro-B cell differentiation | IEA | biological_process |
GO:0002360 | T cell lineage commitment | IEA | biological_process |
GO:0003677 | DNA binding | IEA | molecular_function |
GO:0004672 | Protein kinase activity | TAS | molecular_function |
GO:0004674 | Protein serine/threonine kinase activity | IDA | molecular_function |
GO:0004677 | DNA-dependent protein kinase activity | IDA IEA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005524 | ATP binding | IEA | molecular_function |
GO:0005634 | Nucleus | IEA | cellular_component |
GO:0005654 | Nucleoplasm | TAS | cellular_component |
GO:0005667 | Transcription factor complex | IDA | cellular_component |
GO:0005730 | Nucleolus | IEA | cellular_component |
GO:0005829 | Cytosol | TAS | cellular_component |
GO:0005958 | DNA-dependent protein kinase-DNA ligase 4 complex | IDA | cellular_component |
GO:0006281 | DNA repair | TAS | biological_process |
GO:0006302 | Double-strand break repair | IEA TAS | biological_process |
GO:0006303 | Double-strand break repair via nonhomologous end joining | IEA TAS | biological_process |
GO:0006464 | Cellular protein modification process | TAS | biological_process |
GO:0007420 | Brain development | IEA | biological_process |
GO:0007507 | Heart development | IEA | biological_process |
GO:0008134 | Transcription factor binding | IPI | molecular_function |
GO:0008630 | Intrinsic apoptotic signaling pathway in response to DNA damage | IEA | biological_process |
GO:0010332 | Response to gamma radiation | IEA | biological_process |
GO:0016773 | Phosphotransferase activity, alcohol group as acceptor | IEA | molecular_function |
GO:0018105 | Peptidyl-serine phosphorylation | IDA | biological_process |
GO:0019899 | Enzyme binding | IEA | molecular_function |
GO:0031648 | Protein destabilization | IEA | biological_process |
GO:0032481 | Positive regulation of type I interferon production | TAS | biological_process |
GO:0032869 | Cellular response to insulin stimulus | IMP | biological_process |
GO:0033077 | T cell differentiation in thymus | IEA | biological_process |
GO:0033152 | Immunoglobulin V(D)J recombination | IEA | biological_process |
GO:0033153 | T cell receptor V(D)J recombination | IEA | biological_process |
GO:0035234 | Ectopic germ cell programmed cell death | IEA | biological_process |
GO:0043065 | Positive regulation of apoptotic process | IEA | biological_process |
GO:0045087 | Innate immune response | TAS | biological_process |
GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
GO:0070419 | Nonhomologous end joining complex | IDA | cellular_component |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.2670604726 | 0.1069048478 | 0.9634455455 | 0.6258546486 |
- 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 | Down | -0.0212043359 |
GSE13712_SHEAR | Up | 0.1621849668 |
GSE13712_STATIC | Down | -0.0025773845 |
GSE19018 | Down | -0.1568592456 |
GSE19899_A1 | Down | -0.0236365287 |
GSE19899_A2 | Down | -0.3962261782 |
PubMed_21979375_A1 | Up | 0.0371806254 |
PubMed_21979375_A2 | Down | -0.0578727789 |
GSE35957 | Down | -0.3825187093 |
GSE36640 | Down | -0.8987909225 |
GSE54402 | Up | 0.0793920463 |
GSE9593 | Down | -0.1617304746 |
GSE43922 | Down | -0.0459808536 |
GSE24585 | Down | -0.0608175242 |
GSE37065 | Down | -0.4276447908 |
GSE28863_A1 | Up | 1.4514047163 |
GSE28863_A2 | Up | 1.4488232712 |
GSE28863_A3 | Down | -0.1942215556 |
GSE28863_A4 | Up | 0.1090974505 |
GSE48662 | Down | -0.8555928501 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Name | Drug | Accession number |
---|---|---|
SF1126 | DB05210 | - |
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-101-5p | MIMAT0004513 | MIRT005558 | Luciferase reporter assay//qRT-PCR | Functional MTI | 20617180 |
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- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
---|---|---|---|---|---|---|---|
hsa-miR-101-5p | MIMAT0004513 | 1 | hsa-miR-101* | 20617180 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 10 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
25801233 | Changes in the response of MCF-7 cells to ionizing radiation after the combination of ATM and DNA-PK inhibition |
25801233 | The aim of the present study is to evaluate the role of ATM (KU55933) and DNA-PK (NU7441) inhibitors in the repair of double-strand breaks and downstream signaling of DNA damage introduced by ionizing radiation |
25801233 | After ATM inhibitor pretreatment, the cells were more accumulated in the G2 phase, whereas DNA-PK inhibitor application increased the percentage of cells in the G1 phase |
25801233 | ATM and DNA-PK inhibitor application alone increased the sensitivity of MCF-7 cells to ionizing radiation; however, combining both inhibitors together resulted in a further enhancement of cell death |
25801233 | These proteins were not increased in cells pretreated with the ATM inhibitor prior to ionizing radiation exposure, albeit DNA-PK inhibitor application did not affect the amount of proteins detected |
25801233 | Formation of gammaH2AX was found to be ATM and DNA-PK dependent, application of the ATM inhibitor suppressed incidence of gammaH2AX, whereas DNA-PK caused persistence of gammaH2AX |
25801233 | Our results suggest that the further investigation of the ATM inhibitor in combination with the DNA-PK inhibitor as sensitizers preventing cell senescence and promoting cell death in breast carcinoma MCF-7 cells is warranted |
25012820 | We have reported previously that the DNA-PKcs (DNA-dependent protein kinase catalytic subunit)-interacting protein KIP associates with telomerase through an interaction with hTERT (human telomerase reverse transcriptase) |
23184984 | CD158d initiates signaling through DNA-PKcs, Akt, and NF-kappaB for a proinflammatory and proangiogenic response |
22704488 | In this report, we found that Nampt physically associated with CtIP and DNA-PKcs/Ku80, which are key factors in HR and NHEJ, respectively |
22417805 | METHODS AND MATERIALS: The following assays were used to examine the effect of garcinol on the inhibition of DSB repair, including the following: a conventional neutral comet assay; a cell-based assay recently developed by us, in which NHEJ repair of DSBs on chromosomal DNA was evaluated; the micrococcal nuclease sensitivity assay; and immunoblotting for autophosphorylation of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) |
21037379 | Regulatory roles of tankyrase 1 at telomeres and in DNA repair: suppression of T-SCE and stabilization of DNA-PKcs |
21037379 | Additionally, depletion of tankyrase 1 resulted in concomitant and rapid reduction of the nonhomologous end-joining protein DNA-PKcs, while Ku86 and ATM protein levels remained unchanged; DNA-PKcs mRNA levels were also unaffected |
21037379 | We also demonstrated that depletion of tankyrase 1 resulted in proteasome-mediated DNA-PKcs degradation, explaining the associated defective damage response observed; i |
19188702 | The Ku heterodimer is a DNA end-binding protein that promotes the non-homologous end joining (NHEJ) pathway of DNA double strand break (DSB) repair by recruiting the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs) |
19188702 | These cells have reduced telomerase activity and increased sensitivity to ionizing radiation (IR) but no change in their DNA-PK activity or in the DNA end-binding of endogenous Ku |
17674777 | In this work, the effect of wortmannin (WM), an inhibitor of PI-3 kinases, including DNA-dependent protein kinase (DNA-PK), on the rejoining of strand breaks in telomeric DNA induced by H2O2 in HeLa cells was examined |
17674777 | The results show that WM strongly inhibited the rejoining of telomeric DNA strand breaks, and suggest that DNA-PK might be involved in the repair of telomeric DNA damage |
17347130 | The mutagenic potential of non-homologous end joining in the absence of the NHEJ core factors Ku70/80, DNA-PKcs and XRCC4-LigIV |
17347130 | Non-homologous end joining (NHEJ), the major pathway of double-strand break (DSB) repair in mammalian cells, comprises two subpathways: one that requires the three core factors Ku70/80, DNA-PKcs and XRCC4/LigIV (DNA-PK-dependent NHEJ) and the other that is independent of these factors |
17347130 | Using a cell-free NHEJ assay, we have investigated the ability of three Chinese hamster ovary (CHO) mutants deficient in Ku80 (xrs6), DNA-PKcs (XR-C1) and XRCC4 (XR-1) in comparison with CHO-K1 wild-type cells to rejoin non-compatible DSB ends |
17347130 | Both NHEJ efficiency and fidelity are strongly reduced in the mutants with xrs6 and XR-1 exhibiting the strongest reduction and XR-C1 displaying a phenotype intermediate between the wild-type and the other two mutants indicating a non-essential but facilitating role of DNA-PKcs in NHEJ |
15610769 | Second, the signalling pathway connecting telomere uncapping and replicative senescence appears to be the same as the one that is activated by DNA damage: uncapped telomeres activate signalling cascades involving the protein kinases ATM, ATR and, possibly, DNA-PK |
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