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XRCC4 has a negative role in Agrobacterium T-DNA integration.
In a recombinant PNKP (show PNKP ELISA Kits)-XRCC4-LigIV complex, stable binding of PNKP (show PNKP ELISA Kits) requires XRCC4 phosphorylation. Only one PNKP (show PNKP ELISA Kits) protomer binds per XRCC4 dimer. Both the PNKP (show PNKP ELISA Kits) FHA (show CRY2 ELISA Kits) and catalytic domains contact the XRCC4 coiled-coil and LigIV BRCT repeats. Multipoint contacts between PNKP (show PNKP ELISA Kits) and XRCC4-LigIV regulate PNKP (show PNKP ELISA Kits) recruitment and activity within NHEJ.
Data suggest that stimulation of Artemis nuclease/DCLRE1C (show DCLRE1C ELISA Kits) activity by XRCC4-DNA ligase IV (show LIG4 ELISA Kits) hetero-complex and efficiency of blunt-end ligation are determined by structural configurations at the DNA ends. (XRCC4 = X-ray repair cross complementing 4)
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
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)
XRCC4 expression might have an influence on results of radiotherapy for patients with esophageal squamous cell carcinoma.
uterine cervical cancer patients with high Ku86 (show XRCC5 ELISA Kits) and XRCC4 expression had a significantly lower 5-year metastasis-free rate than others.
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)
Genetic Variations in XRCC4 (rs1805377) is not Associated with Hepatocellular Carcinoma in Thai Patients with Hepatitis B Virus Infection.
These results suggested potential usefulness of the phosphorylation status of XRCC4 Ser320 as an indicator of DNA-PK functionality in living cells.
Association between insertion/deletion polymorphism in intron 3 of XRCC4 and susceptibility to type I bipolar disorder
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
Data show that combined deletion of X-ray repair cross-complementing protein 4 (Xrcc4) and tumor suppressor p53 (Trp53 (show TP53 ELISA Kits)) predisposes B cells to lymphomagenesis.
FBXW7 (show FBXW7 ELISA Kits) facilitates nonhomologous end-joining via K63-linked polyubiquitylation of XRCC4 in tumor cells.
The present results collectively indicated that Lys271, but not Lys210, of XRCC4 is required for the nuclear localization of XRCC4 and LIG4 (show LIG4 ELISA Kits) and that the nuclear localizing ability is essential for DSB repair function of XRCC4.
DNA-PK and ATM (show ATM ELISA Kits) acts in parallel upstream of XRCC4, regulating through phosphorylation
XRCC4 C-terminal point mutants, R325F and N326L, are functionally deficient in terms of cell survival after irradiation.
These results establish that nonrecurrent CNVs can be, and frequently are, formed by mechanisms other than Xrcc4-dependent NHEJ.
analysis of the association of radiation-induced XRCC4 with chromatin DNA, by biochemical fractionation
conditional inactivation of the XRCC4 in nestin (show NES ELISA Kits)-expressing neuronal progenitor cells, although leading to no obvious phenotype in a WT background, leads to early onset of neuronally differentiated medulloblastomas (MBs (show NEU2 ELISA Kits)) in a p53 (show TP53 ELISA Kits)-deficient background
The protein encoded by this gene functions together with DNA ligase IV and the DNA-dependent protein kinase in the repair of DNA double-strand break by non-homologous end joining and the completion of V(D)J recombination events. The non-homologous end-joining pathway is required both for normal development and for suppression of tumors. This gene functionally complements XR-1 Chinese hamster ovary cell mutant, which is impaired in DNA double-strand breaks produced by ionizing radiation and restriction enzymes. Alternative transcription initiation and alternative splicing generates several transcript variants.
DNA repair protein XRCC4
, X-ray repair complementing defective repair in Chinese hamster cells 4
, DNA-repair protein XRCC4
, X-ray repair cross complementing protein 4
, X-ray repair cross-complementing protein 4
, X-ray repair, complementing defective, repair in Chinese hamster