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Single nucleotide polymorphisms in the Ku70 gene XRCC6 were independently associated with Elevated Creatine Kinase Levels in Unhealthy Male Nonagenarians.
HTLV-1 infection enhanced the association between Ku70 and stimulator of IFN genes, suggesting that stimulator of IFN genes was involved in Ku70-mediated host defenses against HTLV-1 infection; findings suggest a new sensor that detects HTLV-1 reverse transcription intermediate and controls HTLV-1 replication
Nuclear PTEN interferes with binding of Ku70 at double-strand breaks through post-translational poly(ADP-ribosyl)ation.
Results show that DDB2 (show DDB2 ELISA Kits) is critical for chromatin association of XRCC5 (show XRCC5 ELISA Kits)/6 in the absence of DNA damage and provide evidence that XRCC5 (show XRCC5 ELISA Kits)/6 are functional partners of DDB2 (show DDB2 ELISA Kits) in its transcriptional stimulatory activity.
High KU70 expression is associated with drug resistance in glioblastoma.
These results suggest that Ku-mediated repression of p53 (show TP53 ELISA Kits) mRNA translation constitutes a novel mechanism linking DNA repair and mRNA translation.
VCP removes sterically trapped Ku70/80 rings from DNA in double-strand break repair.
found that the rs228593, rs2267437 and rs1805388 functional polymorphisms probably alter the level of expression of the ATM (show ATM ELISA Kits), XRCC6 and LIG4 (show LIG4 ELISA Kits) genes, respectively, being important in the maintenance of genomic instability in MDS (show PAFAH1B1 ELISA Kits)
Data show that the increased acetylation of Ku autoantigen 70kDa (Ku70) in sirtuin 6 (show SIRT6 ELISA Kits) protein (SIRT6 (show SIRT6 ELISA Kits))-depleted cells disrupt its interaction with Bax (show BAX ELISA Kits) apoptosis regulator protein (Bax (show BAX ELISA Kits)), which finally resulted in Bax (show BAX ELISA Kits) mitochondrial translocalization.
Ku70 (XRCC6) was found to bind directly within the CR4 of E1A (show BCKDHA ELISA Kits) from human adenovirus type 5.
Ku70 is epistatic with XLF and DNA-PKcs and support a model in which inactivation of Ku70 allows DNA lesions to become accessible to alternative DNA repair pathways (other than Classical Non-Homologous End-Joining (C-NHEJ)).
Study found that emphysema occurred in ku70(-/-) mice at the age of three-months old, and that Bax deficiency was able to suppress it. These results suggest that Bax-mediated apoptosis induces emphysema in ku70(-/-) mice.
Bax deficiency appeared to delay the development of emphysema. This study suggests that enhanced Bax activity exacerbates the negative impact of Ku70 deletion
Ku (ku70/ku80 (show XRCC5 ELISA Kits) heterodimer)roles in nonhomologous end joining and base excision repair pathways of DNA repair are overviewed.
A novel role for free Ku70 and free Ku80 (show XRCC5 ELISA Kits) in altering base excision repair.
A novel function of Ku70 essential for colon homeostasis.
Overexpression of Bcl2 rescues the hematopoietic stem cell defect in Ku70-deficient mice by restoration of quiescence.
This study highlights Ku70 as an important player not only in maintaining genomic stability through NHEJ-dependent functions, but also in regulating pancreatic beta-cell proliferation, a novel NHEJ-independent function.
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.
The findings suggest that Artemis (show DCLRE1C ELISA Kits) can work in not only the Ku-dependent repair process, but also the Ku-independent process at DNA double-strand break in living epithelial cells.
The p70/p80 autoantigen is a nuclear complex consisting of two subunits with molecular masses of approximately 70 and 80 kDa. The complex functions as a single-stranded DNA-dependent ATP-dependent helicase. The complex may be involved in the repair of nonhomologous DNA ends such as that required for double-strand break repair, transposition, and V(D)J recombination. High levels of autoantibodies to p70 and p80 have been found in some patients with systemic lupus erythematosus.
ATP-dependent DNA helicase 2 subunit 1
, ATP-dependent DNA helicase II, 70 kDa subunit
, X-ray repair complementing defective repair in Chinese hamster cells 6 (Ku autoantigen, 70kDa)
, X-ray repair cross-complementing protein 6
, 5'-dRP lyase Ku70
, 5'-deoxyribose-5-phosphate lyase Ku70
, 70 kDa subunit of Ku antigen
, ATP-dependent DNA helicase II 70 kDa subunit
, CTC box binding factor 75 kDa subunit
, CTC box-binding factor 75 kDa subunit
, DNA repair protein XRCC6
, Ku autoantigen p70 subunit
, Ku autoantigen, 70kDa
, lupus Ku autoantigen protein p70
, thyroid autoantigen 70kD (Ku antigen)
, thyroid autoantigen 70kDa (Ku antigen)
, thyroid-lupus autoantigen p70
, 5'-dRP/AP lyase Ku70
, Ku p70
, ku autoantigen protein p70 homolog
, thyroid autoantigen 70 kDa
, Ku70 DNA-binding component of DNA-dependent proteinkinase complex (thyroid autoantigen 70 kDa)
, thyroid autoantigen
, X-ray repair cross-complementing protein 5