ArticleMolecular and cellular biology2003
Nonhomologous-end-joining factors regulate DNA repair fidelity during Sleeping Beauty element transposition in mammalian cells.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 83 citations in OpenAlex.
- Tissue-specific DNA repair strategies underlie apparent high transposon activity in the Caenorhabditis elegans soma.G3 (Bethesda, Md.) · 2026Article
- Metabolic engineering of low-pH-tolerant non-model yeast,Metabolic engineering communications · 2023Article
- Whole Genome Analysis of Dizygotic Twins With Autism Reveals Prevalent Transposon Insertion Within Neuronal Regulatory Elements: Potential Implications for Disease Etiology and Clinical Assessment.Journal of autism and developmental disorders · 2023Article
- RASSF1A independence and early galectin-1 upregulation in PIK3CA-induced hepatocarcinogenesis: new therapeutic venues.Molecular oncology · 2022Article
- A single amino acid switch converts the Sleeping Beauty transposase into an efficient unidirectional excisionase with utility in stem cell reprogramming.Nucleic acids research · 2020Article
- DNA-PK facilitatesProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Sleeping Beauty transposon system for genetic etiological research and gene therapy of cancers.Cancer biology & therapy · 2015Review
- Is non-homologous end-joining really an inherently error-prone process?PLoS genetics · 2014Review
- DNA transposon-based gene vehicles - scenes from an evolutionary drive.Journal of biomedical science · 2013Review
- Article
- Efficient sleeping beauty DNA transposition from DNA minicircles.Molecular therapy. Nucleic acids · 2013Article
- Article
- Article
- Pathway choice in DNA double strand break repair: observations of a balancing act.Genome integrity · 2012Article
- Article
- Comparative genomic integration profiling of Sleeping Beauty transposons mobilized with high efficacy from integrase-defective lentiviral vectors in primary human cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- Virion-associated cofactor high-mobility group DNA-binding protein-1 facilitates transposition from the herpes simplex virus/Sleeping Beauty amplicon vector platform.Human gene therapy · 2010Article
- Harnessing transposons for cancer gene discovery.Nature reviews. Cancer · 2010Review
- Hybrid lentiviral vectors.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Herein, we report that the DNA-dependent protein kinase (DNA-PK) regulates the DNA damage introduced during Sleeping Beauty (SB) element excision and reinsertion in mammalian cells. Using both plasmid- and chromosome-based mobility assays, we analyzed the repair of transposase-induced double-stranded DNA breaks in cells deficient in either the DNA-binding subunit of DNA-PK (Ku) or its catalytic subunit (DNA-PKcs). We found that the free 3' overhangs left after SB element excision were efficiently and accurately processed by the major Ku-dependent nonhomologous-end-joining pathway. Rejoining of broken DNA molecules in the absence of Ku resulted in extensive end degradation at the donor site and greatly increased the frequency of recombination with ectopic templates. Therefore, the major DNA-PK-dependent DNA damage response predominates over more-error-prone repair pathways and thereby facilitates high-fidelity DNA repair during transposon mobilization in mammalian cells. Although transposable elements were not found to be efficiently circularized after transposase-mediated excision, DNA-PK deficiency supported more-frequent transposase-mediated element insertion than was found in wild-type controls. We conclude that, based on its ability to regulate excision site junctional diversity and transposon insertion frequency, DNA-PK serves an important protective role during transpositional recombination in mammals.
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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.