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Human XRCC4 Protein expressed in HEK-293 Cells - ABIN2735698
Myers, Maxwell, Wang: Quantification of XRCC and DNA-PK proteins in cancer cell lines and human tumors by LC-MS/MS. in Bioanalysis 2014
XRCC4 has a negative role in Agrobacterium T-DNA integration.
XRCC4 c.1394G>T Single Nucleotide Polymorphism is associated with Breast Cancer Risk.
Transcription factor ZEB1 was found to directly bind to the SBF2-AS1 promoter region to regulate SBF2-AS1 level and affected TMZ resistance in GBM cells. SBF2-AS1 functions as a ceRNA for miR-151a-3p, leading to the disinhibition of its endogenous target, X-ray repair cross complementing 4 (XRCC4), which enhances DSB repair in GBM cells.
UHRF1-mediated XRCC4 upregulation under pathophysiological conditions triggered by RB1 gene inactivation may confer protection against endogenous DNA damages that arise during retinoblastoma development.
The results suggest that XPD G751A, hOGG1 C326G and XRCC4 G1394T gene polymorphisms might play an important role in colorectal carcinogenesis and increase the risk of developing colorectal cancer in the Chinese Han population.
restriction fragment length polymorphism (RFLP) method was used for evaluating of XPD (-751), XRCC4 (-1394 and a variable number of tandem repeats in intron 3), and XRCC1 (-399) genes. A notable contrast was observed in patients with endometrial hyperplasia without atypia (the SH+CH group) and the NE group in terms of XRCC4 (VNTR intron 3) polymorphisms (P=0.026, P=0.018, respectively).
The present results suggest a potential role of XRCC4 Ser260 phosphorylation by DNA-PK in DNA double-strand break repair.
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.
These data imply that the level of XRCC4 expression could be used to predict the effects of apoptosis-inducing drugs in cancer treatment.
Three-locus model of gene-gene interactions OGG1 (rs1052133) * ADPRT (rs1136410) * XRCC4 (rs6869366) was associated with high genotoxic risk in coal miners.
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.
Results showed that eNOS 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 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.
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 may independently or jointly affect survival in chemotherapy-treated gastric cancer (GCa) patients by modulating the gene expression in the tumors.
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.
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)
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 and XRCC4 expression had a significantly lower 5-year metastasis-free rate than others.
This damaging phenotype highlights the functional nexus between Xlf and Xrcc4, which is critical for the completion of NHEJ-dependent mechanisms during mouse development.
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) predisposes B cells to lymphomagenesis.
FBXW7 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 and that the nuclear localizing ability is essential for DSB repair function of XRCC4.
DNA-PK and ATM 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-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
DNA-PK kinase activity results in disassembly of the Ku/DNA ligase IV/Xrcc4 complex
Connection of XRCC4 and the nonhomologous end joining DNA repair pathway to immunoglobulin class switch recombination.
the KU80/XRCC4 pathway is conservative and not intrinsically error-prone but can accommodate non-fully complementary ends at the cost of limited mutagenesis
A report on the chromosomal repair phenotype of XRCC4 null mouse cells.
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.
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.
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