Functionally-associated target antigens in cancer. Defined by
sClusterin is the Ku70 partner that sterically inhibits Bax-dependent cell death after damage in some pathologic conditions. 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 Suppression of Ku70/80 or Lig4 leads to decreased stable transformation and enhanced homologous recombination in rice AyakoNishizawa-Yokoi1,SatokoNonaka1,2,HiroakiSaika1,Yong-IkKwon1,3,KeishiOsakabe1,4 andSeiichiToki1,3 Ku80 is a protein that, in humans, is encoded by the XRCC5 gene. Together, Ku70 and Ku80 make up the Ku heterodimer, which binds to DNA double-strand break ends and is required for the non-homologous end joining (NHEJ) pathway of DNA repair. 1999-05-01 · Ku70/80 gene expression and DNA-dependent protein kinase (DNA-PK) activity do not correlate with double-strand break (dsb) repair capacity and cellular radiosensitivity in normal human fibroblasts. Kasten U, Plottner N, Johansen J, Overgaard J, Dikomey E. Br J Cancer, 79(7-8):1037-1041, 01 Mar 1999 The Ku70 protein is involved in numerous cell functions, the nonhomologous end joining (NHEJ) DNA repair pathway being the best known.
The connection between the Ku70 level and stabilization of β-catenin merits further investigation, which could shed light on possible ways to enhance pancreatic β-cell proliferation. The heterodimer Ku70/80 plays a critical role in DNA repair and cell death induction after damage. The aberrant expression and localization of these proteins fail to control DNA repair and apoptosis. sClusterin is the Ku70 partner that sterically inhibits Bax-dependent cell death after damage in some pathologic conditions. Here we report that KU70 and DNA-PKcs unexpectedly function together during the induction of apoptosis after exposure to high levels of etoposide. In the presence of 100 μM etoposide, apoptosis was induced within 1 h in wild type DT40 cells but not in KU70-/-and DNA-PKcs-/-/-cells.
Work in our lab has shown that a D192A/D195R mutation in helix five of the Ku70 von Willebrand A (vWA) domain leads to an NHEJ defect.
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The mechanism of Ku70/80 detachment from the DNA helix after completion of DNA repair is incompletely understood. The genetic disease Fanconi anemia (FA) results from mutations in a series of genes involved in a DNA repair pathway that helps process the damage caused by erroneous chemical cross-links between the two strands of the DNA double helix. The double-stranded breaks in DNA that arise from such cross-links can be repaired in an error-free manner or through an error-prone repair pathway.
Functional organisation of the cell nucleus in the fission - DiVA
Supplied as 500 µL purified antibody (0.2 mg/mL). of the Ku70/80 heterodimer in vitro. We further deﬁned the function of the Ku70 and Ku80 C-terminal domains in DNA end binding and DNA-PKCS interaction. 2. Results 2.1.
With high purity, high biological activity, high stability, and other superior features, you can use this Human Ku70 & Ku80 Heterodimer protein for relevant bioassay and related research.
Required for mating-type switching (By similarity). 1999-01-01 Invitrogen Anti-Ku70/Ku80 Monoclonal (162), Catalog # MA1-21818.
As DNA end joining would be detrimental to chromosome ends, it was though that Ku has to be kept away from telomeres to prevent deleterious telomere-telomere fusion. This study highlights Ku70 as an important player not only in maintaining genomic stability through NHEJ-dependent functions, but also in regulating pancreatic β-cell proliferation, a novel NHEJ-independent function. Indeed, Ku70/80 has been proposed to perform at least two functions at telomeres.
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