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Ku (ku70 (show XRCC6 Proteins)/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 (show MLXIP Proteins)-31.
Inactivation of Ku80 and DNA-PKCS (show PRKDC Proteins) causes reduced lifespan and bodyweight.
A novel role for free Ku70 (show XRCC6 Proteins) and free Ku80 in altering base excision repair.
Ku80 plays an important role in base excision repair.
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 (show XRCC6 Proteins)/86 binds to the Apaf1 (show APAF1 Proteins) 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.
SAF-A (show HNRNPU Proteins), 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 (show CASP2 Proteins)-mediated Ku80 cleavage promotes Ku80/DNA-PKcs (show PRKDC Proteins) interaction as the D726A mutation diminished Ku80 interaction with DNA-PKcs (show PRKDC Proteins)
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 (show CALCR Proteins) (C-terminal region) is required for interaction with DNA-PKcs (show PRKDC Proteins) 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 (show PRKDC Proteins)-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 (show EP300 Proteins) to regulate COX-2 expression, and suggested that the XRCC5/p300 (show EP300 Proteins)/COX-2 signaling pathway was a potential target in the treatment of colon cancers
Ku antigen displays the AP lyase (show APEX1 Proteins) activity on a certain type of double-stranded DNA.
Results show that DDB2 (show DDB2 Proteins) 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 (show DDB2 Proteins) 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.
VCP/p97 (show vcp Proteins) extracts sterically trapped Ku70 (show XRCC6 Proteins)/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