ArticleScience advances2019
Nuclear receptors regulate alternative lengthening of telomeres through a novel noncanonical FANCD2 pathway.
Article in Science advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Twisting the End Game: How Telomere Chromatin Modifications Shape Telomere Maintenance.Aging cell · 2026Review
- Orphan nuclear receptors recruit TRIM28 to promote telomeric H3K9me3 for the ALT pathway.The EMBO journal · 2026Article
- RNA G-Quadruplex RIBOTAC-Mediated Targeted Degradation of lncRNA TERRA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multiple functions of the ALT favorite helicase, BLM.Cell & bioscience · 2025Review
- Lipid Profiles, Telomere Length, and the Risk of Malignant Tumors: A Mendelian Randomization and Mediation Analysis.Biomedicines · 2024Article
- Orphan nuclear receptors-induced ALT-associated PML bodies are targets for ALT inhibition.Nucleic acids research · 2024Article
- Article
- The Altered Functions of Shelterin Components in ALT Cells.International journal of molecular sciences · 2023Review
- Review
- DNA methylation changes in glial cells of the normal-appearing white matter in Multiple Sclerosis patients.Epigenetics · 2022Article
- Telomeric replication stress: the beginning and the end for alternative lengthening of telomeres cancers.Open biology · 2022Review
- Article
- Regulation of Replication Stress in Alternative Lengthening of Telomeres by Fanconi Anaemia Protein.Genes · 2022Review
- Anti-recombination function of MutSα restricts telomere extension by ALT-associated homology-directed repair.Cell reports · 2021Article
- Alternative lengthening of telomeres in molecular subgroups of paediatric high-grade glioma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Article
- The absence of (TCAGGG)Scientific reports · 2020Article
- Alternative Lengthening of Telomeres: Building Bridges To Connect Chromosome Ends.Trends in cancer · 2020Review
- ALT: A Multi-Faceted Phenomenon.Genes · 2020Review
- Alternative lengthening of telomeres: from molecular mechanisms to therapeutic outlooks.Cell & bioscience · 2020Review
- Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Alternative lengthening of telomeres (ALT) is known to use homologous recombination (HR) to replicate telomeric DNA in a telomerase-independent manner. However, the detailed process remains largely undefined. It was reported that nuclear receptors COUP-TFII and TR4 are recruited to the enriched GGGTCA variant repeats embedded within ALT telomeres, implicating nuclear receptors in regulating ALT activity. Here, we identified a function of nuclear receptors in ALT telomere maintenance that involves a direct interaction between COUP-TFII/TR4 and FANCD2, the key protein in the Fanconi anemia (FA) DNA repair pathway. The COUP-TFII/TR4-FANCD2 complex actively induces the DNA damage response by recruiting endonuclease MUS81 and promoting the loading of the PCNA-POLD3 replication complex in ALT telomeres. Furthermore, the COUP-TFII/TR4-mediated ALT telomere pathway does not require the FA core complex or the monoubiquitylation of FANCD2, key steps in the canonical FA pathway. Thus, our findings reveal that COUP-TFII/TR4 regulates ALT telomere maintenance through a novel noncanonical FANCD2 pathway.
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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.