HCSGD entry for XRCC6
1. General information
Official gene symbol | XRCC6 |
---|---|
Entrez ID | 2547 |
Gene full name | X-ray repair complementing defective repair in Chinese hamster cells 6 |
Other gene symbols | CTC75 CTCBF G22P1 KU70 ML8 TLAA |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
![color bar](img/red_blue.jpg)
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0000723 | Telomere maintenance | IEA TAS | biological_process |
GO:0000783 | Nuclear telomere cap complex | TAS | cellular_component |
GO:0003677 | DNA binding | NAS | molecular_function |
GO:0003684 | Damaged DNA binding | IEA | molecular_function |
GO:0003690 | Double-stranded DNA binding | TAS | molecular_function |
GO:0003691 | Double-stranded telomeric DNA binding | IDA | molecular_function |
GO:0004003 | ATP-dependent DNA helicase activity | IEA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005524 | ATP binding | IEA | molecular_function |
GO:0005634 | Nucleus | TAS | cellular_component |
GO:0005654 | Nucleoplasm | TAS | cellular_component |
GO:0005667 | Transcription factor complex | IDA | cellular_component |
GO:0005730 | Nucleolus | IEA | cellular_component |
GO:0005737 | Cytoplasm | IEA | cellular_component |
GO:0005829 | Cytosol | TAS | cellular_component |
GO:0006200 | ATP catabolic process | TAS | biological_process |
GO:0006266 | DNA ligation | TAS | biological_process |
GO:0006281 | DNA repair | TAS | biological_process |
GO:0006302 | Double-strand break repair | TAS | biological_process |
GO:0006303 | Double-strand break repair via nonhomologous end joining | IEA IMP TAS | biological_process |
GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
GO:0007420 | Brain development | IEA | biological_process |
GO:0008022 | Protein C-terminus binding | IPI | molecular_function |
GO:0016020 | Membrane | TAS | cellular_component |
GO:0016032 | Viral process | TAS | biological_process |
GO:0032481 | Positive regulation of type I interferon production | TAS | biological_process |
GO:0032508 | DNA duplex unwinding | TAS | biological_process |
GO:0033151 | V(D)J recombination | IEA | biological_process |
GO:0042162 | Telomeric DNA binding | IEA | molecular_function |
GO:0043564 | Ku70:Ku80 complex | IDA IEA | cellular_component |
GO:0044212 | Transcription regulatory region DNA binding | IDA | molecular_function |
GO:0045087 | Innate immune response | TAS | biological_process |
GO:0045892 | Negative regulation of transcription, DNA-templated | IMP | biological_process |
GO:0045893 | Positive regulation of transcription, DNA-templated | IDA IMP | biological_process |
GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
GO:0050769 | Positive regulation of neurogenesis | IEA | biological_process |
GO:0051575 | 5'-deoxyribose-5-phosphate lyase activity | IMP | molecular_function |
GO:0070419 | Nonhomologous end joining complex | IDA | cellular_component |
GO:0071475 | Cellular hyperosmotic salinity response | IEA | biological_process |
GO:0071481 | Cellular response to X-ray | IEA | biological_process |
GO:0075713 | Establishment of integrated proviral latency | TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.8440766574 | 0.3930878424 | 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 | Up | 0.3984522282 |
GSE13712_SHEAR | Up | 0.0814608904 |
GSE13712_STATIC | Down | -0.0490187797 |
GSE19018 | Down | -0.0190413135 |
GSE19899_A1 | Down | -0.2018421486 |
GSE19899_A2 | Up | 0.0921404987 |
PubMed_21979375_A1 | Up | 0.0106593307 |
PubMed_21979375_A2 | Down | -0.0185065875 |
GSE35957 | Down | -0.1502162237 |
GSE36640 | Down | -0.3183307294 |
GSE54402 | Up | 0.1192789185 |
GSE9593 | Down | -0.1623414688 |
GSE43922 | Down | -0.1138588319 |
GSE24585 | Down | -0.1264235308 |
GSE37065 | Down | -0.0129686747 |
GSE28863_A1 | Up | 0.0948899556 |
GSE28863_A2 | Down | -0.1722897463 |
GSE28863_A3 | Down | -0.1312996249 |
GSE28863_A4 | Up | 0.1516481211 |
GSE48662 | Down | -0.1276712036 |
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-941 | MIMAT0004984 | MIRT036579 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-877-3p | MIMAT0004950 | MIRT036849 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-766-3p | MIMAT0003888 | MIRT039005 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-671-5p | MIMAT0003880 | MIRT039281 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-615-3p | MIMAT0003283 | MIRT039688 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-505-3p | MIMAT0002876 | MIRT041064 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-193b-3p | MIMAT0002819 | MIRT041244 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-484 | MIMAT0002174 | MIRT041722 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-423-3p | MIMAT0001340 | MIRT042559 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-324-3p | MIMAT0000762 | MIRT042905 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-326 | MIMAT0000756 | MIRT043624 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-128-3p | MIMAT0000424 | MIRT045877 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-221-3p | MIMAT0000278 | MIRT046859 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-181b-5p | MIMAT0000257 | MIRT047271 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-100-5p | MIMAT0000098 | MIRT048583 | CLASH | Functional 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: 15 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27302174 | Ku70 is essential for non-homologous end joining pathway for DNA double strand break repair, and Bax plays an important role in apoptosis |
26224580 | Statins also impaired the expression of DNA repair genes, including XRCC4, XRCC6, and Apex1 |
25582120 | Mechanistically, telomere fusions require either the classical non-homologous end-joining (C-NHEJ) pathway dependent on Ku70/80 and LIG4, or the alternative non-homologous end-joining (A-NHEJ), which relies on PARP1 and LIG3 |
24816985 | Moreover, TERT bound to PTTG1 formed complexes with chaperones such as Ku70 and heat shock protein 90 |
24816985 | The interaction between TERT and PTTG1 by association of Ku70 might be important for the enhancement of the limited self-renewal activity of MSCs and for understanding the regulatory mechanisms of self-renewal |
24322375 | Induction of cellular senescence by RD occurred through activation of DNA damage response including increases in the phosphor-H2AX, inactivation of Chk1/2, and suppression of repair-related Ku70/86 and phosphor-BRCA1 in PCa cells in vitro and in vivo |
24244594 | To 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 |
24244594 | We found that the level of gammaH2AX was increased, whereas the level of Ku70 was reduced in lungs of CS-exposed mice |
24244594 | Furthermore, p21 deletion reduced the level of gammaH2AX, but augmented the levels of Ku70, Ku80, and PAR in lungs by CS |
23474484 | Ku70 functions in addition to nonhomologous end joining in pancreatic beta-cells: a connection to beta-catenin regulation |
23474484 | In the present study, to further delineate the function of NHEJ, we analyzed mice deficient for another key NHEJ factor, Ku70, to discover the effect of cellular responses to DNA damage in pancreatic beta-cells on cellular proliferation and glucose homeostasis |
23474484 | To our surprise, Ku70(-/-) mice had significantly increased beta-cell proliferation and islet expansion, heightened insulin levels, and decreased glycemia |
23474484 | This study highlights Ku70 as an important player not only in maintaining genomic stability through NHEJ-dependent functions, but also in regulating pancreatic beta-cell proliferation, a novel NHEJ-independent function |
23299825 | Toll-like receptor 4 activity protects against hepatocellular tumorigenesis and progression by regulating expression of DNA repair protein Ku70 in mice |
23299825 | Moreover, TLR4 mutation resulted in a suppressed capacity of DNA repair due to a decrease in TLR4-medicated expression of DNA repair proteins Ku70/80 in liver tissue and cells |
21512205 | Depletion of Ku70/80 reduces the levels of extrachromosomal telomeric circles and inhibits proliferation of ALT cells |
21512205 | Here we show that shRNA-mediated knockdown of the Ku70/80 heterodimer, a factor with functions at both pathological and natural DNA ends, inhibits ALT cell growth and results in a significant decrease in the levels of t-circles without affecting overall telomere length |
20148697 | Lentivirus-mediated RNA interference of Ku70 to enhance radiosensitivity of human mammary epithelial cells |
20148697 | PURPOSE: 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 |
20148697 | MATERIALS AND METHODS: MCF10A cells were infected with lentiviral vectors for RNAi of Ku70 |
20148697 | RESULTS: Western blot analysis showed that the Ku70 lentiviral vector was effective in silencing the expression of both Ku70 and Ku80 |
20148697 | RNAi of Ku70 also resulted in a lower survival yield after irradiation compared to the control cell line |
20148697 | CONCLUSION: RNAi of Ku70 resulted in increased chromosomal and cellular radiosensitivity in the MCF10A human mammary cell line after irradiation with (60)Co gamma-rays |
19948976 | Exercise upregulated telomerase activity in the thoracic aorta and in circulating mononuclear cells compared with sedentary controls, increased vascular expression of telomere repeat-binding factor 2 and Ku70, and reduced the expression of vascular apoptosis regulators such as cell-cycle-checkpoint kinase 2, p16, and p53 |
17686666 | Here, we show that the levels of Ku70 and Ku80 drop approximately twofold in replicatively senescent cells |
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 |
17202845 | Decreased expression of DNA repair proteins Ku70 and Mre11 is associated with aging and may contribute to the cellular senescence |
17202845 | Our data presented here show that among the DSB repair proteins tested, only the expression of Ku70 and Mre11 showed statistically significant age-dependent changes in human lymphocytes |
17202845 | Furthermore, we found that expressions of Ku70 and Mre11 are statistically correlated, which indicate that the function of Ku70 and Mre11 may be related |
17202845 | In line with these data, people who live in the regional community (longevity group), which was found to have statistically longer average life span than the rest area, shows higher level of Ku70 expression than those living in the neighboring control community |
17202845 | Taken together, our data show, for the first time, that Ku70 and Mre11 may represent new biomarkers for aging and further suggest that maintenance of higher expression of Ku70 and Mre11 may be responsible for keeping longer life span observed in the longevity group |
10606813 | The activity is elevated in late-passaged and senescent cells, and the cleaved 69-kDa product seems able to form complex with Ku70 to bind DNA ends |
10606813 | In fact, the levels of Ku86, Ku70 and DNA-end binding activity of Ku remained unchanged during replicative senescence |
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