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XRCC4 has a negative role in Agrobacterium T-DNA integration.
Association between insertion/deletion polymorphism in intron 3 of XRCC4 and susceptibility to type I bipolar disorder
For XRCC4 (rs1805377) polymorphism, no difference was found in distribution between the ESCC and control groups.
using dual- and quadruple-trap optical tweezers combined with fluorescence microscopy, we show how human XRCC4, XLF (show NHEJ1 ELISA Kits) and XRCC4-XLF (show NHEJ1 ELISA Kits) complexes interact with DNA in real time
The ends are then closely aligned, which requires XLF (show NHEJ1 ELISA Kits), a non-catalytic function of XRCC4-LIG4 (show LIG4 ELISA Kits), and DNA-PK activity
Polymorphisms of XRCC4 are associated with susceptibility to Colorectal Cancer.
FBXW7 (show FBXW7 ELISA Kits) facilitates nonhomologous end-joining via K63-linked polyubiquitylation of XRCC4 in tumor cells.
The XRCC4 -1394T/G polymorphism is associated with susceptibility to endometriosis in an Iranian population.
Our results suggest that the XRCC4 rs2075685 polymorphism could influence the susceptibility to pancreatic cancer in a Chinese population.
The TMPRSS2 (show TMPRSS2 ELISA Kits)-ERG (show ERG ELISA Kits) Gene Fusion Blocks XRCC4-Mediated Nonhomologous End-Joining Repair and Radiosensitizes Prostate Cancer Cells to PARP (show COL11A2 ELISA Kits) Inhibition
Point mutations in XRCC4 is associated with microcephaly, short stature and genomic instability.
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.
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
DNA-PK kinase activity results in disassembly of the Ku/DNA ligase IV (show LIG4 ELISA Kits)/Xrcc4 complex
Connection of XRCC4 and the nonhomologous end joining DNA repair pathway to immunoglobulin class switch recombination.
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