Browse our anti-XRCC4 (XRCC4) Antibodies

Arabidopsis thaliana X-Ray Repair Complementing Defective Repair in Chinese Hamster Cells 4 (XRCC4) interaction partners

1. XRCC4 has a negative role in Agrobacterium T-DNA integration.

Human X-Ray Repair Complementing Defective Repair in Chinese Hamster Cells 4 (XRCC4) interaction partners

1. PAXX, XLF and XRCC4 synergise in the efficient DNA double-strand breaks recruitment, substrate recognition and stimulation of Pol lambda enzymatic activity during nonhomologous end joining DNA repair.

2. These data imply that the level of XRCC4 expression could be used to predict the effects of apoptosis-inducing drugs in cancer treatment.

3. Three-locus model of gene-gene interactions OGG1 (rs1052133) * ADPRT (rs1136410) * XRCC4 (rs6869366) was associated with high genotoxic risk in coal miners.

4. Variant rs3734091 was found to be significantly associated with breast cancer while rs6869366 variant did not show any association. These SNPs may influence the susceptibility of individuals to breast cancer in this Indian population.

5. Results showed that eNOS and XRCC4 VNTR variants might play a potential role in schizophrenia + nicotine dependence and/or nicotine dependence pathophysiology.

6. Phospho-blocking and -mimicking mutations impact both the stability and DNA bridging capacity of XRCC4/XLF complexes, but without affecting their ability to stimulate LIG4 activity. Implicit in this finding is that phosphorylation may regulate DNA bridging by XRCC4/XLF filaments.

7. This study demonstrated both ligase IV and XRCC4 may act in concert to modulate the development of glioma.

8. Data suggest that genetic variants of XRCC4 and ERCC1 may independently or jointly affect survival in chemotherapy-treated gastric cancer (GCa) patients by modulating the gene expression in the tumors.

9. In a recombinant PNKP-XRCC4-LigIV complex, stable binding of PNKP requires XRCC4 phosphorylation. Only one PNKP protomer binds per XRCC4 dimer. Both the PNKP FHA and catalytic domains contact the XRCC4 coiled-coil and LigIV BRCT repeats. Multipoint contacts between PNKP and XRCC4-LigIV regulate PNKP recruitment and activity within NHEJ.

10. Data suggest that stimulation of Artemis nuclease/DCLRE1C activity by XRCC4-DNA ligase IV hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 = X-ray repair cross complementing 4)

11. involvement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the expression of genes that act in different repair mechanisms

12. the various XRCC4 mutations that lead to primordial dwarfism and their impact on non-homologous end joining and V(D)J recombination are discussed (Review)

13. XRCC4 expression might have an influence on results of radiotherapy for patients with esophageal squamous cell carcinoma.

14. uterine cervical cancer patients with high Ku86 and XRCC4 expression had a significantly lower 5-year metastasis-free rate than others.

15. Frequencies of XRCC4-1394 T/G+G/G genotypes were higher in patients (%34) than the controls (%18.7). The statistical analysis revealed that the individuals who had XRCC4-1394 T/G+G/G genotype had an increased risk for autism spectrum disorder (OR = 2.23, 95% CI = 1.10-4.55)

16. Genetic Variations in XRCC4 (rs1805377) is not Associated with Hepatocellular Carcinoma in Thai Patients with Hepatitis B Virus Infection.

17. These results suggested potential usefulness of the phosphorylation status of XRCC4 Ser320 as an indicator of DNA-PK functionality in living cells.

18. Association between insertion/deletion polymorphism in intron 3 of XRCC4 and susceptibility to type I bipolar disorder

19. For XRCC4 (rs1805377) polymorphism, no difference was found in distribution between the ESCC and control groups.

20. using dual- and quadruple-trap optical tweezers combined with fluorescence microscopy, we show how human XRCC4, XLF and XRCC4-XLF complexes interact with DNA in real time

Mouse (Murine) X-Ray Repair Complementing Defective Repair in Chinese Hamster Cells 4 (XRCC4) interaction partners

1. These data imply that the level of XRCC4 expression could be used to predict the effects of apoptosis-inducing drugs in cancer treatment.

2. involvement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the expression of genes that act in different repair mechanisms

3. We find that non-canonical HR termination can occur in the absence of the classical non-homologous end joining gene XRCC4. We observe obligatory use of microhomology (MH)-mediated end joining and/or nucleotide addition during rejoining with the second end of the break

4. Data show that combined deletion of X-ray repair cross-complementing protein 4 (Xrcc4) and tumor suppressor p53 (Trp53) predisposes B cells to lymphomagenesis.

5. FBXW7 facilitates nonhomologous end-joining via K63-linked polyubiquitylation of XRCC4 in tumor cells.

6. The present results collectively indicated that Lys271, but not Lys210, of XRCC4 is required for the nuclear localization of XRCC4 and LIG4 and that the nuclear localizing ability is essential for DSB repair function of XRCC4.

7. DNA-PK and ATM acts in parallel upstream of XRCC4, regulating through phosphorylation

8. XRCC4 C-terminal point mutants, R325F and N326L, are functionally deficient in terms of cell survival after irradiation.

9. These results establish that nonrecurrent CNVs can be, and frequently are, formed by mechanisms other than Xrcc4-dependent NHEJ.

10. analysis of the association of radiation-induced XRCC4 with chromatin DNA, by biochemical fractionation

11. conditional inactivation of the XRCC4 in nestin-expressing neuronal progenitor cells, although leading to no obvious phenotype in a WT background, leads to early onset of neuronally differentiated medulloblastomas (MBs) in a p53-deficient background

12. DNA-PK kinase activity results in disassembly of the Ku/DNA ligase IV/Xrcc4 complex

13. Connection of XRCC4 and the nonhomologous end joining DNA repair pathway to immunoglobulin class switch recombination.

14. the KU80/XRCC4 pathway is conservative and not intrinsically error-prone but can accommodate non-fully complementary ends at the cost of limited mutagenesis

15. A report on the chromosomal repair phenotype of XRCC4 null mouse cells.

16. Data suggest that Xrcc4/p53-deficient pro-B lymphomas routinely activate c-myc by gene amplification, whereas Xrcc4/p53-deficient peripheral B cell lymphomas routinely ectopically activate a single c-myc copy.

17. Data show that depletion of Mre11 reduces the use of microhomology during NHEJ in Xrcc4(+/+) cells and suppresses end resection in Xrcc4(-/-) cells, revealing specific roles for Mre11 in both classical and alternative NHEJ.