HCSGD entry for XRCC5


1. General information

Official gene symbolXRCC5
Entrez ID7520
Gene full nameX-ray repair complementing defective repair in Chinese hamster cells 5 (double-strand-break rejoining)
Other gene symbolsKARP-1 KARP1 KU80 KUB2 Ku86 NFIV
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 maintenanceIEA TASbiological_process
GO:0000783Nuclear telomere cap complexTAScellular_component
GO:0000784Nuclear chromosome, telomeric regionIDAcellular_component
GO:0003677DNA bindingNASmolecular_function
GO:0003684Damaged DNA bindingIEAmolecular_function
GO:0003690Double-stranded DNA bindingTASmolecular_function
GO:0003691Double-stranded telomeric DNA bindingIDAmolecular_function
GO:0004003ATP-dependent DNA helicase activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005524ATP bindingIEAmolecular_function
GO:0005634NucleusIDAcellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0005730NucleolusIDAcellular_component
GO:0005737CytoplasmIEAcellular_component
GO:0005829CytosolTAScellular_component
GO:0006200ATP catabolic processTASbiological_process
GO:0006281DNA repairTASbiological_process
GO:0006302Double-strand break repairTASbiological_process
GO:0006303Double-strand break repair via nonhomologous end joiningIEA IMP TASbiological_process
GO:0006310DNA recombinationIEAbiological_process
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0007420Brain developmentIEAbiological_process
GO:0008022Protein C-terminus bindingIPImolecular_function
GO:0008283Cell proliferationIEAbiological_process
GO:0016032Viral processTASbiological_process
GO:0031625Ubiquitin protein ligase bindingIPImolecular_function
GO:0032481Positive regulation of type I interferon productionTASbiological_process
GO:0032508DNA duplex unwindingTASbiological_process
GO:0042162Telomeric DNA bindingIDA IEAmolecular_function
GO:0042493Response to drugIEAbiological_process
GO:0043564Ku70:Ku80 complexIDA IEAcellular_component
GO:0044212Transcription regulatory region DNA bindingIDAmolecular_function
GO:0045087Innate immune responseTASbiological_process
GO:0045892Negative regulation of transcription, DNA-templatedIMPbiological_process
GO:0050769Positive regulation of neurogenesisIEAbiological_process
GO:00515755'-deoxyribose-5-phosphate lyase activityIMPmolecular_function
GO:0060218Hematopoietic stem cell differentiationIEAbiological_process
GO:0070419Nonhomologous end joining complexIDAcellular_component
GO:0071398Cellular response to fatty acidIEAbiological_process
GO:0071475Cellular hyperosmotic salinity responseIEAbiological_process
GO:0071481Cellular response to X-rayIEAbiological_process
GO:0075713Establishment of integrated proviral latencyTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.92751552750.09725864900.99999024730.5950592515

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

Data sourceUp or downLog fold change
GSE11954Down-0.0090738673
GSE13712_SHEARDown-0.0989363617
GSE13712_STATICDown-0.1711361819
GSE19018Down-0.3090137602
GSE19899_A1Down-0.1171027001
GSE19899_A2Down-0.5113956313
PubMed_21979375_A1Down-0.0387297201
PubMed_21979375_A2Down-0.3156885596
GSE35957Down-0.2234644801
GSE36640Down-0.6454331409
GSE54402Up0.2487661100
GSE9593Down-0.4015682478
GSE43922Down-0.0203219227
GSE24585Down-0.0833451565
GSE37065Up0.0399369557
GSE28863_A1Up0.2826961929
GSE28863_A2Up0.6171097487
GSE28863_A3Down-0.0010364224
GSE28863_A4Down-0.0330038133
GSE48662Down-0.6322352844

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-484MIMAT0002174MIRT042031CLASHFunctional MTI (Weak)23622248
hsa-miR-331-3pMIMAT0000760MIRT043483CLASHFunctional MTI (Weak)23622248
hsa-miR-7-5pMIMAT0000252MIRT047762CLASHFunctional MTI (Weak)23622248
hsa-miR-100-5pMIMAT0000098MIRT048471CLASHFunctional MTI (Weak)23622248
hsa-miR-26b-5pMIMAT0000083MIRT050041CLASHFunctional MTI (Weak)23622248
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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: 16 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

24244594To test this hypothesis, we determined the levels of gammaH2AX (a marker for DNA double-strand breaks) as well as non-homologous end joining proteins (Ku70 and Ku80) in lungs of mice exposed to CS
24244594Furthermore, p21 deletion reduced the level of gammaH2AX, but augmented the levels of Ku70, Ku80, and PAR in lungs by CS
21469181E(2) had no regulatory effects on the expression rates of the cell cycle regulator p21 and the DNA repair proteins SIRT1 and XRCC5
21376036SIRT1 and XRCC5 were up-regulated after oxidant insult and expression levels increased in aging cells
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
20148697PURPOSE: To investigate the radiosensitising effect of Ku autoantigen 70 (Ku70) and Ku autoantigen 80 (Ku80) knockdown by lentivirus-mediated RNA interference (RNAi) in the MCF10A immortalised human mammary epithelial cell line
20148697RESULTS: Western blot analysis showed that the Ku70 lentiviral vector was effective in silencing the expression of both Ku70 and Ku80
19946467Here we showed that Ku86 deficiency accelerated the high NaCl-induced cellular senescence
19946467We find that 1) high NaCl induces rapid cellular senescence in Ku86 deficient(xrs5) cells, 2) Ku86 deficiency shortens lifespan of C
19946467Further, although water balance is known to be compromised in old mice, this occurs at much earlier age in Ku86(-/-) mice
19946467When subjected to mild water restriction, 3 month old Ku86(-/-), but not Ku86(+/+),mice rapidly become dehydrated as evidenced by decrease in body weight, increased production of antidiuretic hormone,increased urine osmolality and decreased urine volume
19946467We conclude that Ku86 deficiency accelerates high NaCl(-) induced cellular senescence,particularly in the renal medulla where NaCl normally is high
19597334Ku80 is often referred to as a tumor suppressor since it maintains the genome by repairing DNA double-strand breaks (DSBs) via the nonhomologous end joining (NHEJ) pathway
19597334Even though Ku80 deletion causes hypersensitivity to gamma-radiation, DNA damage and chromosomal rearrangements, Ku80-mutant mice exhibit very low cancer levels
19597334In addition, Ku80 and p53 show a genetic interaction to suppress pro-B cell lymphoma and medulloblastoma
19535900Recently, we reported the effect of loss of function of p21, a gene implicated in p53-induced cellular senescence, in the background of the Ku80(-/-) premature aging mouse (Zhao et al
19188702Here we describe human cells that express fusions between the large human Ku subunit (Ku86) and a fluorescent protein tag
19188702These data are consistent with models in which Ku recruits telomerase to telomeres or activates recruited telomerase and suggest that the Ku86 fusion proteins specifically block this role
19079133Ku80 is important in the repair of DNA double-strand breaks by its essential function in non-homologous end-joining
19079133The absence of Ku80 causes the accumulation of DNA damage and leads to premature ageing in mice
18941635Effect of Ku80 deficiency on mutation frequencies and spectra at a LacZ reporter locus in mouse tissues and cells
18941635Indeed, we found a substantial increase in persistent 53BP1 and gammaH2AX DNA damage foci in Ku80-/- as compared to wild-type liver
17686666Here, we show that the levels of Ku70 and Ku80 drop approximately twofold in replicatively senescent cells
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
17202845All the other DSB repair proteins tested, Sir2, TRF1 and Ku80, did not show any significant differences upon aging
17173483Interestingly, a similar perturbation of the postnatal growth axis was not detected in another progeroid mouse model, the double-strand DNA break repair deficient Ku80(-/-) mouse
10606813Senescent human fibroblasts have elevated Ku86 proteolytic cleavage activity
10606813However, further studies indicate that cleavage of Ku86 could be inhibited by including leupeptin in the extraction buffer, and no 69 kDa variant was evident in the cell
10606813In fact, the levels of Ku86, Ku70 and DNA-end binding activity of Ku remained unchanged during replicative senescence
10606813Thus, this study reveals an intriguing protease in HDFs, and also indicates that inconsistent results of Ku86 expression will be obtained if the protease activity is not completely inhibited
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