ArticleNature communications2020
The nuclear pore complex prevents sister chromatid recombination during replicative senescence.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- RNA export through the nuclear pore complex: pathways, mechanisms, and imaging strategies.RNA biology · 2026Review
- The nuclear pore complex as a spatial organizing hub for high-risk DNA lesions.Nucleus (Austin, Tex.) · 2026Review
- Ctf18-dependent localization of interstitial telomeric sequence to nuclear pore complexes prevents chromosome fragility.Nucleic acids research · 2026Article
- The role of the nuclear pore complex in the stability of disease-related short tandem DNA repeats.Nucleic acids research · 2026Article
- Cruciform-forming AT/TA repeats are acted upon by structure-selective endonucleases and Rad51 prior to repositioning to the nuclear periphery for repair.Nucleic acids research · 2026Article
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- The DNA replication checkpoint targets the kinetochore to reposition DNA structure-induced replication damage to the nuclear periphery.Cell reports · 2025Article
- Nucleoporins cooperate with Polycomb silencers to promote transcriptional repression and repair at DNA double-strand breaks.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The DNA damage tolerance factor Rad5 and telomere replication.Current genetics · 2025Review
- The fission yeast SUMO-targeted ubiquitin ligase Slx8 functionally associates with clustered centromeres and the silent mating-type region at the nuclear periphery.Biology open · 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
- SUMO protease and proteasome recruitment at the nuclear periphery differently affect replication dynamics at arrested forks.Nucleic acids research · 2024Article
- Improved detection of DNA replication fork-associated proteins.Cell reports · 2024Article
- STIM1 translocation to the nucleus protects cells from DNA damage.Nucleic acids research · 2024Article
- Extracellular vesicles derived from mesenchymal stem cells: the wine in Hebe's hands to treat skin aging.Precision clinical medicine · 2024Review
- TERRA R-loops connect and protect sister telomeres in mitosis.Cell reports · 2023Article
- A R-loop sensing pathway mediates the relocation of transcribed genes to nuclear pore complexes.Nature communications · 2023Article
- NPCs and APBs: two HUBs of non-canonical homology-based recombination at telomeres?Cell cycle (Georgetown, Tex.) · 2023Article
- Article
- Structure, Maintenance, and Regulation of Nuclear Pore Complexes: The Gatekeepers of the Eukaryotic Genome.Cold Spring Harbor perspectives in biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The Nuclear Pore Complex (NPC) has emerged as an important hub for processing various types of DNA damage. Here, we uncover that fusing a DNA binding domain to the NPC basket protein Nup1 reduces telomere relocalization to nuclear pores early after telomerase inactivation. This Nup1 modification also impairs the relocalization to the NPC of expanded CAG/CTG triplet repeats. Strikingly, telomerase negative cells bypass senescence when expressing this Nup1 modification by maintaining a minimal telomere length compatible with proliferation through rampant unequal exchanges between sister chromatids. We further report that a Nup1 mutant lacking 36 C-terminal residues recapitulates the phenotypes of the Nup1-LexA fusion indicating a direct role of Nup1 in the relocation of stalled forks to NPCs and restriction of error-prone recombination between repeated sequences. Our results reveal a new mode of telomere maintenance that could shed light on how 20% of cancer cells are maintained without telomerase or ALT.
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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.