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anti-Human XRCC4 Antibodies:
anti-Mouse (Murine) XRCC4 Antibodies:
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Human Polyclonal XRCC4 Primary Antibody for IHC - ABIN967264
Li, Otevrel, Gao, Cheng, Seed, Stamato, Taccioli, Alt: The XRCC4 gene encodes a novel protein involved in DNA double-strand break repair and V(D)J recombination. in Cell 1996
Show all 5 Pubmed References
Human Polyclonal XRCC4 Primary Antibody for IHC - ABIN967265
Leber, Wise, Mizuta, Meek: The XRCC4 gene product is a target for and interacts with the DNA-dependent protein kinase. in The Journal of biological chemistry 1998
Show all 5 Pubmed References
Human Polyclonal XRCC4 Primary Antibody for ICC, IF - ABIN4366467
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
Show all 2 Pubmed References
Mouse (Murine) Polyclonal XRCC4 Primary Antibody for IHC, WB - ABIN3022382
Dong, Wang, Wang, Zhang, Zhu, Gao, Yang, Qin, Liang, Chen, Deng, Ning, Liang, Gao, Xu: A stress-induced cellular aging model with postnatal neural stem cells. in Cell death & disease 2014
Human Polyclonal XRCC4 Primary Antibody for IF, IHC (p) - ABIN1327721
Enervald, Du, Visnes, Björkman, Lindgren, Wincent, Borck, Colleaux, Cormier-Daire, van Gent, Pie, Puisac, de Miranda, Kracker, Hammarström, de Villartay, Durandy, Schoumans, Ström, Pan-Hammarström: A regulatory role for the cohesin loader NIPBL in nonhomologous end joining during immunoglobulin class switch recombination. in The Journal of experimental medicine 2013
Human Polyclonal XRCC4 Primary Antibody for ICC, IF - ABIN440923
van Sluis, McStay: A localized nucleolar DNA damage response facilitates recruitment of the homology-directed repair machinery independent of cell cycle stage. in Genes & development 2015
XRCC4 has a negative role in Agrobacterium T-DNA integration.
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.
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.
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.
This study demonstrated both ligase IV and XRCC4 may act in concert to modulate the development of glioma.
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.
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.
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)
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
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.
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 Antibodies)) predisposes B cells to lymphomagenesis.
FBXW7 (show FBXW7 Antibodies) 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 Antibodies) and that the nuclear localizing ability is essential for DSB repair function of XRCC4.
DNA-PK and ATM (show ATM Antibodies) 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 Antibodies)-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 Antibodies)) in a p53 (show TP53 Antibodies)-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