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

2. Three-locus model of gene-gene interactions OGG1 (show OGG1 Antibodies) (rs1052133) * ADPRT (show PARP1 Antibodies) (rs1136410) * XRCC4 (rs6869366) was associated with high genotoxic risk in coal miners.

3. Results showed that eNOS (show NOS3 Antibodies) and XRCC4 VNTR variants might play a potential role in schizophrenia + nicotine dependence and/or nicotine dependence pathophysiology.

4. Phospho-blocking and -mimicking mutations impact both the stability and DNA bridging capacity of XRCC4/XLF (show NHEJ1 Antibodies) complexes, but without affecting their ability to stimulate LIG4 (show LIG4 Antibodies) activity. Implicit in this finding is that phosphorylation may regulate DNA bridging by XRCC4/XLF (show NHEJ1 Antibodies) filaments.

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

6. Data suggest that genetic variants of XRCC4 and ERCC1 (show ERCC1 Antibodies) may independently or jointly affect survival in chemotherapy-treated gastric cancer (GCa (show NPR1 Antibodies)) patients by modulating the gene expression in the tumors.

7. In a recombinant PNKP (show PNKP Antibodies)-XRCC4-LigIV complex, stable binding of PNKP (show PNKP Antibodies) requires XRCC4 phosphorylation. Only one PNKP (show PNKP Antibodies) protomer binds per XRCC4 dimer. Both the PNKP (show PNKP Antibodies) FHA (show CRY2 Antibodies) and catalytic domains contact the XRCC4 coiled-coil and LigIV BRCT repeats. Multipoint contacts between PNKP (show PNKP Antibodies) and XRCC4-LigIV regulate PNKP (show PNKP Antibodies) recruitment and activity within NHEJ.

8. Data suggest that stimulation of Artemis nuclease/DCLRE1C (show DCLRE1C Antibodies) activity by XRCC4-DNA ligase IV (show LIG4 Antibodies) hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 = X-ray repair cross complementing 4)

9. involvement of ZNF281 (show ZNF281 Antibodies) in the cellular response to genotoxic stress through the control exercised on the expression of genes that act in different repair mechanisms

10. 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)

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 (show ZNF281 Antibodies) 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 (show TP53 Antibodies)) predisposes B cells to lymphomagenesis.

5. FBXW7 (show FBXW7 Antibodies) 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 (show LIG4 Antibodies) and that the nuclear localizing ability is essential for DSB repair function of XRCC4.

7. DNA-PK and ATM (show ATM Antibodies) 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