ArticleDNA repair2011
Subtelomeric regions in mammalian cells are deficient in DNA double-strand break repair.
Article in DNA repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed.
- The hierarchical stratum response system of organism to microgravity during spaceflight.Military Medical Research · 2026Review
- Article
- Changes in Telomere Length in Leukocytes and Leukemic Cells after Ultrashort Electron Beam Radiation.International journal of molecular sciences · 2024Article
- Telomeric RNA (TERRA) increases in response to spaceflight and high-altitude climbing.Communications biology · 2024Article
- Telomeres and aging: on and off the planet!Biogerontology · 2024Review
- High-throughput screen to identify compounds that prevent or target telomere loss in human cancer cells.NAR cancer · 2022Article
- The contribution of DNA repair pathways to genome editing and evolution in filamentous pathogens.FEMS microbiology reviews · 2022Review
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
- Telomeric Double Strand Breaks in G1 Human Cells Facilitate Formation of 5' C-Rich Overhangs and Recruitment of TERRA.Frontiers in genetics · 2021Article
- Dysfunctional telomeres trigger cellular senescence mediated by cyclic GMP-AMP synthase.The Journal of biological chemistry · 2020Article
- Mild Telomere Dysfunction as a Force for Altering the Adaptive Potential of Subtelomeric Genes.Genetics · 2018Article
- Review
- Differences in the recruitment of DNA repair proteins at subtelomeric and interstitial I-SceI endonuclease-induced DNA double-strand breaks.DNA repair · 2017Article
- Telomere-Internal Double-Strand Breaks Are Repaired by Homologous Recombination and PARP1/Lig3-Dependent End-Joining.Cell reports · 2016Article
- Homologous recombination-dependent repair of telomeric DSBs in proliferating human cells.Nature communications · 2016Article
- Sister chromatid telomere fusions, but not NHEJ-mediated inter-chromosomal telomere fusions, occur independently of DNA ligases 3 and 4.Genome research · 2016Article
- Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.Nucleic acids research · 2015Article
- Targeted DNA damage at individual telomeres disrupts their integrity and triggers cell death.Nucleic acids research · 2015Article
- De Novo ring chromosome 11 and non-reciprocal translocation of 11p15.3-pter to 21qter in a patient with congenital heart disease.Molecular cytogenetics · 2015Article
- The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
We have previously demonstrated that double-strand breaks (DSBs) in regions near telomeres are much more likely to result in large deletions, gross chromosome rearrangements, and chromosome instability than DSBs at interstitial sites within chromosomes. In the present study, we investigated whether this response of subtelomeric regions to DSBs is a result of a deficiency in DSB repair by comparing the frequency of homologous recombination repair (HRR) and nonhomologous end joining (NHEJ) at interstitial and telomeric sites following the introduction of DSBs by I-SceI endonuclease. We also monitored the frequency of small deletions, which have been shown to be the most common mutation at I-SceI-induced DSBs at interstitial sites. We observed no difference in the frequency of small deletions or HRR at interstitial and subtelomeric DSBs. However, the frequency of NHEJ was significantly lower at DSBs near telomeres compared to interstitial sites. The frequency of NHEJ was also lower at DSBs occurring at interstitial sites containing telomeric repeat sequences. We propose that regions near telomeres are deficient in classical NHEJ as a result of the presence of cis-acting telomere-binding proteins that cause DSBs to be processed as though they were telomeres, resulting in excessive resection, telomere loss, and eventual chromosome rearrangements by alternative NHEJ.
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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.