HCSGD entry for PRKDC


1. General information

Official gene symbolPRKDC
Entrez ID5591
Gene full nameprotein kinase, DNA-activated, catalytic polypeptide
Other gene symbolsDNA-PKcs DNAPK DNPK1 HYRC HYRC1 XRCC7 p350
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000723Telomere maintenanceIEAbiological_process
GO:0001756SomitogenesisIEAbiological_process
GO:0002326B cell lineage commitmentIEAbiological_process
GO:0002328Pro-B cell differentiationIEAbiological_process
GO:0002360T cell lineage commitmentIEAbiological_process
GO:0003677DNA bindingIEAmolecular_function
GO:0004672Protein kinase activityTASmolecular_function
GO:0004674Protein serine/threonine kinase activityIDAmolecular_function
GO:0004677DNA-dependent protein kinase activityIDA IEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005524ATP bindingIEAmolecular_function
GO:0005634NucleusIEAcellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0005667Transcription factor complexIDAcellular_component
GO:0005730NucleolusIEAcellular_component
GO:0005829CytosolTAScellular_component
GO:0005958DNA-dependent protein kinase-DNA ligase 4 complexIDAcellular_component
GO:0006281DNA repairTASbiological_process
GO:0006302Double-strand break repairIEA TASbiological_process
GO:0006303Double-strand break repair via nonhomologous end joiningIEA TASbiological_process
GO:0006464Cellular protein modification processTASbiological_process
GO:0007420Brain developmentIEAbiological_process
GO:0007507Heart developmentIEAbiological_process
GO:0008134Transcription factor bindingIPImolecular_function
GO:0008630Intrinsic apoptotic signaling pathway in response to DNA damageIEAbiological_process
GO:0010332Response to gamma radiationIEAbiological_process
GO:0016773Phosphotransferase activity, alcohol group as acceptorIEAmolecular_function
GO:0018105Peptidyl-serine phosphorylationIDAbiological_process
GO:0019899Enzyme bindingIEAmolecular_function
GO:0031648Protein destabilizationIEAbiological_process
GO:0032481Positive regulation of type I interferon productionTASbiological_process
GO:0032869Cellular response to insulin stimulusIMPbiological_process
GO:0033077T cell differentiation in thymusIEAbiological_process
GO:0033152Immunoglobulin V(D)J recombinationIEAbiological_process
GO:0033153T cell receptor V(D)J recombinationIEAbiological_process
GO:0035234Ectopic germ cell programmed cell deathIEAbiological_process
GO:0043065Positive regulation of apoptotic processIEAbiological_process
GO:0045087Innate immune responseTASbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIMPbiological_process
GO:0070419Nonhomologous end joining complexIDAcellular_component
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.26706047260.10690484780.96344554550.6258546486

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

Data sourceUp or downLog fold change
GSE11954Down-0.0212043359
GSE13712_SHEARUp0.1621849668
GSE13712_STATICDown-0.0025773845
GSE19018Down-0.1568592456
GSE19899_A1Down-0.0236365287
GSE19899_A2Down-0.3962261782
PubMed_21979375_A1Up0.0371806254
PubMed_21979375_A2Down-0.0578727789
GSE35957Down-0.3825187093
GSE36640Down-0.8987909225
GSE54402Up0.0793920463
GSE9593Down-0.1617304746
GSE43922Down-0.0459808536
GSE24585Down-0.0608175242
GSE37065Down-0.4276447908
GSE28863_A1Up1.4514047163
GSE28863_A2Up1.4488232712
GSE28863_A3Down-0.1942215556
GSE28863_A4Up0.1090974505
GSE48662Down-0.8555928501

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

SF1126DB05210 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-101-5pMIMAT0004513MIRT005558Luciferase reporter assay//qRT-PCRFunctional MTI20617180
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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-101-5pMIMAT00045131hsa-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

25801233Changes in the response of MCF-7 cells to ionizing radiation after the combination of ATM and DNA-PK inhibition
25801233The 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
25801233After 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
25801233ATM 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
25801233These 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
25801233Formation 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
25801233Our 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
25012820We 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)
23184984CD158d initiates signaling through DNA-PKcs, Akt, and NF-kappaB for a proinflammatory and proangiogenic response
22704488In this report, we found that Nampt physically associated with CtIP and DNA-PKcs/Ku80, which are key factors in HR and NHEJ, respectively
22417805METHODS 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)
21037379Regulatory roles of tankyrase 1 at telomeres and in DNA repair: suppression of T-SCE and stabilization of DNA-PKcs
21037379Additionally, 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
21037379We also demonstrated that depletion of tankyrase 1 resulted in proteasome-mediated DNA-PKcs degradation, explaining the associated defective damage response observed; i
19188702The 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)
19188702These 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
17674777In 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
17674777The 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
17347130The mutagenic potential of non-homologous end joining in the absence of the NHEJ core factors Ku70/80, DNA-PKcs and XRCC4-LigIV
17347130Non-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
17347130Using 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
17347130Both 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
15610769Second, 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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