ArticleMutation research
Ku80-deleted cells are defective at base excision repair.
Article in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Systematic evaluation of the DNA repair machinery facilitated the development of efficient genome editing tools for the red yeastSynthetic and systems biotechnology · 2027Article
- Genotoxicity-Stimulated and CYLD-Driven Malignant Transformation.Cancer management and research · 2022Article
- Causes and Effects of Loss of Classical Nonhomologous End Joining Pathway in Parasitic Eukaryotes.mBio · 2019Article
- Physiological functions of programmed DNA breaks in signal-induced transcription.Nature reviews. Molecular cell biology · 2017Review
- Investigation into experimental toxicological properties of plant protection products having a potential link to Parkinson's disease and childhood leukaemia.EFSA journal. European Food Safety Authority · 2017Article
- Combined Effects of High-Dose Bisphenol A and Oxidizing Agent (KBrO3) on Cellular Microenvironment, Gene Expression, and Chromatin Structure of Ku70-deficient Mouse Embryonic Fibroblasts.Environmental health perspectives · 2016Article
- Identification of a conserved 5'-dRP lyase activity in bacterial DNA repair ligase D and its potential role in base excision repair.Nucleic acids research · 2016Article
- Common cancer-associated imbalances in the DNA damage response confer sensitivity to single agent ATR inhibition.Oncotarget · 2015Article
- Article
- Bisphenol a promotes cell survival following oxidative DNA damage in mouse fibroblasts.PloS one · 2015Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Ku80 forms a heterodimer with Ku70, called Ku, that repairs DNA double-strand breaks (DSBs) via the nonhomologous end joining (NHEJ) pathway. As a consequence of deleting NHEJ, Ku80-mutant cells are hypersensitive to agents that cause DNA DSBs like ionizing radiation. Here we show that Ku80 deletion also decreased resistance to ROS and alkylating agents that typically cause base lesions and single-strand breaks (SSBs). This is unusual since base excision repair (BER), not NHEJ, typically repairs these types of lesions. However, we show that deletion of another NHEJ protein, DNA ligase IV (Lig4), did not cause hypersensitivity to these agents. In addition, the ROS and alkylating agents did not induce γ-H2AX foci that are diagnostic of DSBs. Furthermore, deletion of Ku80, but not Lig4 or Ku70, reduced BER capacity. Ku80 deletion also impaired BER at the initial lesion recognition/strand scission step; thus, involvement of a DSB is unlikely. Therefore, our data suggests that Ku80 deletion impairs BER via a mechanism that does not repair DSBs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.