ArticlePloS one2014
The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Correlation Between the Clinical and Histopathological Results in Experimental Sciatic Nerve Defect Surgery.Medicina (Kaunas, Lithuania) · 2025Article
- Xrcc5/Ku80 is required for the repair of DNA damage in fully grown meiotically arrested mammalian oocytes.Cell death & disease · 2023Article
- Pathological consequences of DNA damage in the kidney.Nature reviews. Nephrology · 2023Review
- DNA damage-induced degradation of Sp1 promotes cellular senescence.GeroScience · 2022Article
- Synergistic radiosensitizing effect of BR101801, a specific DNA-dependent protein kinase inhibitor, in various human solid cancer cells and xenografts.American journal of cancer research · 2021Article
- Ku86 alleviates human umbilical vein endothelial cellular apoptosis and senescence induced by a low dose of ionizing radiation.The Journal of international medical research · 2019Article
- Constitutive Dicer1 phosphorylation accelerates metabolism and aging in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Do p53 stress responses impact organismal aging?Translational cancer research · 2016Article
- Do DNA Double-Strand Breaks Drive Aging?Molecular cell · 2016Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Ku80 and DNA-PKCS are both involved in the repair of double strand DNA breaks via the nonhomologous end joining (NHEJ) pathway. While ku80-/- mice exhibit a severely reduced lifespan and size, this phenotype is less pronounced in dna-pkcs-/- mice. However, these observations are based on independent studies with varying genetic backgrounds. Here, we generated ku80-/-, dna-pkcs-/- and double knock out mice in a C57Bl6/J*FVB F1 hybrid background and compared their lifespan, end of life pathology and mutation frequency in liver and spleen using a lacZ reporter. Our data confirm that inactivation of Ku80 and DNA-PKCS causes reduced lifespan and bodyweights, which is most severe in ku80-/- mice. All mutant mice exhibited a strong increase in lymphoma incidence as well as other aging-related pathology (skin epidermal and adnexal atrophy, trabacular bone reduction, kidney tubular anisokaryosis, and cortical and medullar atrophy) and severe lymphoid depletion. LacZ mutation frequency analysis did not show strong differences in mutation frequencies between knock out and wild type mice. The ku80-/- mice had the most severe phenotype and the Ku80-mutation was dominant over the DNA-PKCS-mutation. Presumably, the more severe degenerative effect of Ku80 inactivation on lifespan compared to DNA-PKCS inactivation is caused by additional functions of Ku80 or activity of free Ku70 since both Ku80 and DNA-PKCS are essential for NHEJ.
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