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RT-PCR and immunobloting data show that inhibitory effect of sodium butyrate takes place at the level of Rad51 and XRCC5 gene transcription and the content of Rad51 and Ku80 proteins.
Ku (ku70/ku80 heterodimer)roles in nonhomologous end joining and base excision repair pathways of DNA repair are overviewed.
the downregulation of Ku80 and an impairment of repair activity in squamous cells, which are mediated by miR-31.
Inactivation of Ku80 and DNA-PKCS causes reduced lifespan and bodyweight.
A novel role for free Ku70 and free Ku80 in altering base excision repair.
Ku80 plays an important role in base excision repair.
Loss of a single allele is sufficient to accelerate aging in skeletal muscle although post-natal growth is normal.
Ku70/80 binds to DNA double strand breaks (DSB) in all cell cycle stages and is likely actively displaced from DSB ends to free the DNA ends for DNA end resection and thus homologous recombination to occur.
There was a dose-dependent and time-dependent increase in Ku80 mRNA levels in nude mice that were inoculated with A549 cells and exposed to varying doses of irradiation.
Ku70/86 binds to the Apaf1 promoter and represses its activity.
Mobility of a major portion of Ku80 is not affected by DNA double strans breaks (DSBs) in order to find other DSBs in hamster cells.
It was concluded that Ku86 deficiency accelerates high NaCl induced cellular senescence in cultured cells, C. elegans, and knockout mouse kidney.
Data show that Ku80 reactivation in retinal neurocytes by 5-azacytidine enhances DNA integrity after treatment with H(2)O(2).
Data show that DSB promote PP2A to associate with Ku 70 and Ku 86.
Ku80 is required for Galpha13-mediated endodermal differentiation in P19 cells
mice doubly deficient for telomerase and either Ku86 or DNA-PKcs manifest accelerated loss of organismal viability compared with single telomerase-deficient mice.
Knockout mice may develop telomere dysfunction and organismal premature aging.
sites within the imprinting control center of the H19 and Igf2 genes bind Ku70/80 in a sequence-specific manner and with higher affinity than previously reported binding sites
The deficiency of Ku80 resulted in a prolonged G1 phase, as well as decreased Ku binding to and activation of origins of DNA replication.
Ku86 ameliorates the effects of high NaCl-induced DNA breaks in adapted cells by supporting alignment of the broken ends of the DNA and thus maintaining integrity of the fragmented chromatin.
The crystal structures of the Ku-binding motifs (KBM) of the non-homologous end joining (NHEJ) proteins APLF (A-KBM) and XLF (X-KBM) bound to a Ku-DNA complex are discussed.
Ku80 overexpression associates with unfavorable prognosis of superficial ESCC patients, and silencing of Ku80 could inhibit the malignant behavior of ESCC cells. We provide evidence that Ku80 has unrecognized roles in carcinogenesis and development of ESCC.
ATM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nuclease activities are required to limit the stable loading of Ku on single-ended DNA double-strand breaks.
these results suggest that polymorphisms of XRCC5 play an important role in astrocytoma prognosis in the Chinese Han population which could be used in the determination of astrocytoma prognosis in clinical researches
SAF-A, in concert with Ku, temporally regulates base damage repair in irradiated cell genome.
High XRCC5 expresiion is associated with medullary thyroid carcinoma.
Ku80 can be cleaved by caspases-2 at D726 upon a transient etoposide treatment. Caspase-2-mediated Ku80 cleavage promotes Ku80/DNA-PKcs interaction as the D726A mutation diminished Ku80 interaction with DNA-PKcs
m-calpain translocated as the result of calcium influx was involved in DNA double-strand breaks repair, especially in the non-homologous end-joining pathway through proteolysis of nuclear Ku80. Cleaved Ku80 was still able to form a heterodimer with Ku70 and enhance DNA repair activity.
Ku80 CTR (C-terminal region) is required for interaction with DNA-PKcs on short segments of blunt ended 25bp dsDNA or 25bp dsDNA with a 15-base poly dA ssDNA extension, but this requirement is less stringent on longer dsDNA molecules (35bp blunt ended dsDNA) or 25bp duplex DNA with either a 15-base poly dT or poly dC ssDNA extension. Moreover, DNA-PKcs-Ku complex forms on 25 bp DNA with poly-pyrimidine ssDNA extension.
Ku80 could predict the probability of resistance to neoadjuvant chemotherapy in lung adenocarcinoma, and reduced cisplatin and pemetrexed-induced apoptosis in A549 cells
results demonstrated that XRCC5 promoted colon cancer growth by cooperating with p300 to regulate COX-2 expression, and suggested that the XRCC5/p300/COX-2 signaling pathway was a potential target in the treatment of colon cancers
Ku antigen displays the AP lyase activity on a certain type of double-stranded DNA.
Results show that DDB2 is critical for chromatin association of XRCC5/6 in the absence of DNA damage and provide evidence that XRCC5/6 are functional partners of DDB2 in its transcriptional stimulatory activity.
RNF126 is a novel regulator of NHEJ that promotes completion of DNA repair by ubiquitylating Ku80 and releasing Ku70/80 from damaged DNA.
uterine cervical cancer patients with high Ku86 and XRCC4 expression had a significantly lower 5-year metastasis-free rate than others.
XRCC5 (rs1051685, rs6941) and AQP2 (10875989, rs3759125) polymorphisms were associated with hematologic toxicity of platinum-based chemotherapy in lung cancer patients
Ku80 and PDGFR-alpha might be effective predictive indicators for the prognosis of nasal type NK/T cell lymphoma
DNA methylation modification plays an important role to regulate the gene expression of XRCC5 and XRCC7, from the results that the gene methylation level of the glioma group is higher than that of the normal group
Data suggest that heat shock factor 1 (HSF1) interacts with both Ku autoantigens Ku70 and Ku86 to induce defective non-homologous end joining (NHEJ) repair activity and genomic instability.
The present study showed that the XRCC5 locus might be a contributor to COPD susceptibility in the Chinese Han population.
VCP/p97 extracts sterically trapped Ku70/80 rings from DNA in double-strand break repair.
Double strand break (DSB)-induced ubiquitylation of Ku80 provides a mechanism to efficiently eliminate Ku from DNA for pre- and postrepair processes.
The protein encoded by this gene is the 80-kilodalton subunit of the Ku heterodimer protein which is also known as ATP-dependant DNA helicase II or DNA repair protein XRCC5. Ku is the DNA-binding component of the DNA-dependent protein kinase, and it functions together with the DNA ligase IV-XRCC4 complex in the repair of DNA double-strand break by non-homologous end joining and the completion of V(D)J recombination events. This gene functionally complements Chinese hamster xrs-6, a mutant defective in DNA double-strand break repair and in ability to undergo V(D)J recombination. A rare microsatellite polymorphism in this gene is associated with cancer in patients of varying radiosensitivity.
, X-ray repair complementing defective repair in Chinese hamster cells 5 (double-strand-break rejoining; Ku autoantigen, 80kDa)
, X-ray repair protein
, X-ray repair cross-complementing protein 5
, X-ray repair complementing defective repair in Chinese hamster cells 5 (double-strand-break rejoining)
, ATP-dependent DNA helicase II
, ATP-dependent DNA helicase 2 subunit 2-like
, x-ray repair cross-complementing protein 5-like
, ATP-dependent DNA helicase 2 subunit 2
, ATP-dependent DNA helicase II 80 kDa subunit
, CTC box-binding factor 85 kDa subunit
, DNA repair protein XRCC5
, Ku p80
, ku autoantigen protein p86 homolog
, nuclear factor IV
, Ku autoantigen, 80kD)
, X-ray repair cross complementation (double-strand-break rejoining
, X-ray repair cross complementation (double-strand-break rejoining; Ku autoantigen, 80kD)
, 86 kDa subunit of Ku antigen
, Ku autoantigen, 80kDa
, Ku86 autoantigen related protein 1
, lupus Ku autoantigen protein p86
, thyroid-lupus autoantigen
, X-ray repair complementing defective repair in Chinese hamster cells 5