ArticleNature communications2016
Homologous recombination-dependent repair of telomeric DSBs in proliferating human cells.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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
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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Efficacy and Safety of PARP Inhibitor Therapy in Advanced Ovarian Cancer: A Systematic Review and Network Meta-analysis of Randomized Controlled Trials.Current computer-aided drug design · 2024Pooled it
- Selective killing of ALT-cancer cells by Withaferin-A involves destabilization of Rad51 and disruption of DNA repair.Cell death & disease · 2026Article
- SIRT2 mitigates radiation-induced oral mucositis by promoting homologous recombination-mediated DNA double-strand break repair in epithelial stem cells.Cancer letters · 2026Article
- Fmp45 promotes Rad53 dephosphorylation via Ptc2 interaction to attenuate checkpoint signaling and maintain genome stability.Journal, genetic engineering & biotechnology · 2025Article
- Applications of CRISPR-Cas9 in mitigating cellular senescence and age-related disease progression.Clinical and experimental medicine · 2025Review
- Premature aging and metabolic diseases: the impact of telomere attrition.Frontiers in aging · 2025Review
- LAP2α orchestrates alternative lengthening of telomeres suppression through telomeric heterochromatin regulation with HDAC1: unveiling a potential therapeutic target.Cell death & disease · 2024Article
- Telomeric DNA breaks in human induced pluripotent stem cells trigger ATR-mediated arrest and telomerase-independent telomere damage repair.Journal of molecular cell biology · 2024Article
- Aging, Cancer, and Inflammation: The Telomerase Connection.International journal of molecular sciences · 2024Review
- Therapy-induced senescence through the redox lens.Redox biology · 2024Review
- The crosstalk between telomeres and DNA repair mechanisms: an overview to mammalian somatic cells, germ cells, and preimplantation embryos.Journal of assisted reproduction and genetics · 2024Review
- RBMX involves in telomere stability maintenance by regulating TERRA expression.PLoS genetics · 2023Article
- Mapping cellular responses to DNA double-strand breaks using CRISPR technologies.Trends in genetics : TIG · 2023Review
- Article
- Amplification and Quantitation of Telomeric Extrachromosomal Circles.Bio-protocol · 2023Article
- BMAL1 collaborates with CLOCK to directly promote DNA double-strand break repair and tumor chemoresistance.Oncogene · 2023Article
- Phosphorylation of TRF2 promotes its interaction with TIN2 and regulates DNA damage response at telomeres.Nucleic acids research · 2023Article
- DNA Damage Response-Associated Cell Cycle Re-Entry and Neuronal Senescence in Brain Aging and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- High-throughput screen to identify compounds that prevent or target telomere loss in human cancer cells.NAR cancer · 2022Article
- METTL3-mediated m6A modification stabilizes TERRA and maintains telomere stability.Nucleic acids research · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomeres prevent chromosome ends from being recognized as double-stranded breaks (DSBs). Meanwhile, G/C-rich repetitive telomeric DNA is susceptible to attack by DNA-damaging agents. How cells balance the need to protect DNA ends and the need to repair DNA lesions in telomeres is unknown. Here we show that telomeric DSBs are efficiently repaired in proliferating cells, but are irreparable in stress-induced and replicatively senescent cells. Using the CRISPR-Cas9 technique, we specifically induce DSBs at telomeric or subtelomeric regions. We find that DSB repair (DSBR) at subtelomeres occurs in an error-prone manner resulting in small deletions, suggestive of NHEJ. However, DSBR in telomeres involves 'telomere-clustering', 3'-protruding C-rich telomeric ssDNA, and HR between sister-chromatid or interchromosomal telomeres. DSBR in telomeres is suppressed by deletion or inhibition of Rad51. These findings reveal proliferation-dependent DSBR in telomeres and suggest that telomeric HR, which is normally constitutively suppressed, is activated in the context of DSBR.
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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.