ArticleProceedings of the National Academy of Sciences of the United States of America2004
DNA end joining becomes less efficient and more error-prone during cellular senescence.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.
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Who cites it
181 citing papers in PubMed, 275 citations in OpenAlex.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Translational control by RPL22L1-specific ribosomes enhances DNA repair and chemoresistance.Nature communications · 2026Article
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- Mechanistic redundancy and hierarchy of aging mechanisms: implications for strategies to extend healthspan and biomarker integration.Frontiers in aging · 2026Review
- Defining aging-associated factors that increase susceptibility to prostate cancer.Endocrine-related cancer · 2025Review
- Synergistic enhancement of PARP inhibition via small molecule UNI66-mediated suppression of BRD4-dependent transcription ofNAR cancer · 2025Article
- RNA demethylase ALKBH5 regulates cell cycle progression in DNA damage response.Scientific reports · 2025Article
- Nuclear accumulation of YTHDF1 regulates mRNA splicing in the DNA damage response.Science advances · 2025Article
- Age-dependent cytokine surge in blood precedes cancer diagnosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ACSS2 drives senescence-associated secretory phenotype by limiting purine biosynthesis through PAICS acetylation.Nature communications · 2025Article
- Article
- Amodiaquine ameliorates stress-induced premature cellular senescence via promoting SIRT1-mediated HR repair.Cell death discovery · 2024Article
- Review
- Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation.bioRxiv : the preprint server for biology · 2024Article
- GCN5 mediates DNA-PKcs crotonylation for DNA double-strand break repair and determining cancer radiosensitivity.British journal of cancer · 2024Article
- Kaposi's sarcoma herpesvirus exploits the DNA damage response to circularize its genome.Nucleic acids research · 2024Article
- PKCδ Regulates Chromatin Remodeling and DNA Repair through SIRT6.Molecular cancer research : MCR · 2024Article
- Effects of p53 and ATRX inhibition on telomeric recombination in aging fibroblasts.Frontiers in oncology · 2024Article
- Progerin can induce DNA damage in the absence of global changes in replication or cell proliferation.PloS one · 2024Article
- Androgen signaling stabilizes genomes to counteract senescence by promoting XRCC4 transcription.EMBO reports · 2023Article
121 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulation of somatic mutations is thought to contribute to the aging process. Genomic instability has been shown to increase during aging, suggesting an aberrant function of DNA double-strand break (DSB) repair. Surprisingly, DSB repair has not been examined with respect to cellular senescence. Therefore, we have studied the ability of young, presenescent, and senescent normal human fibroblasts to repair DSBs in transfected DNA by using a fluorescent reporter substrate. We have found that the efficiency of end joining is reduced up to 4.5 fold in presenescent and senescent cells, relative to young cells. Sequence analysis of end junctions showed that the frequency of precise ligation was higher in young cells, whereas end joining in old cells was associated with extended deletions. These results indicate that end joining becomes inefficient and more error-prone during cellular senescence. Furthermore, the ability to use microhomologies for end joining was compromised in senescent cells, suggesting that young and senescent cells may use different end joining pathways. We hypothesize that inefficient and aberrant end joining is a likely mechanism underlying the age-related genomic instability and higher incidence of cancer in the elderly.
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