ArticleNucleic acids research2009
Stabilization of quadruplex DNA perturbs telomere replication leading to the activation of an ATR-dependent ATM signaling pathway.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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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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
86 citing papers in PubMed, 172 citations in OpenAlex.
- Inhibition of lagging strand replication by G-rich telomeric DNA and the shelterin subunit POT1.The EMBO journal · 2026Article
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Targeted therapies in pediatric oncology: A start.Molecular therapy. Oncology · 2026Review
- BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.Communications biology · 2026Article
- Modulating TERRA G-quadruplexes with ligands: impact on telomeric DNA:RNA hybrids and ALT mechanisms.Nucleic acids research · 2025Article
- The effect of prolonged G-quadruplex stabilization on the functions of human cells.Scientific reports · 2025Article
- Recent Progress and Potential of G4 Ligands in Cancer Immunotherapy.Molecules (Basel, Switzerland) · 2025Review
- Review
- Pursuing Polypharmacology: Benzothiopyranoindoles as G-Quadruplex Stabilizers and Topoisomerase I Inhibitors for Effective Anticancer Strategies.ACS medicinal chemistry letters · 2024Article
- Joint Efforts of Replicative Helicase and SSB Ensure Inherent Replicative Tolerance of G-Quadruplex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- G-quadruplex formation within the promoter region ofHeliyon · 2024Article
- Application of G-quadruplex targets in gastrointestinal cancers: Advancements, challenges and prospects.World journal of gastrointestinal oncology · 2023Review
- PARP1 allows proper telomere replication through TRF1 poly (ADP-ribosyl)ation and helicase recruitment.Communications biology · 2023Article
- Review
- Identifying and Differentiating Topological G-Quadruplex Structures with DNA-Encoded Plasmonic Gold Nanoparticles.Angewandte Chemie (International ed. in English) · 2022Article
- Ligands stimulating antitumour immunity as the next G-quadruplex challenge.Molecular cancer · 2022Review
- Article
- From telomere to telomere: The transcriptional and epigenetic state of human repeat elements.Science (New York, N.Y.) · 2022Article
- Reversal of G-Quadruplexes' Role in Translation Control When Present in the Context of an IRES.Biomolecules · 2022Review
- Transcriptional regulation of telomeric repeat-containing RNA by acridine derivatives.RNA biology · 2021Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Functional telomeres are required to maintain the replicative ability of cancer cells and represent putative targets for G-quadruplex (G4) ligands. Here, we show that the pentacyclic acridinium salt RHPS4, one of the most effective and selective G4 ligands, triggers damages in cells traversing S phase by interfering with telomere replication. Indeed, we found that RHPS4 markedly reduced BrdU incorporation at telomeres and altered the dynamic association of the telomeric proteins TRF1, TRF2 and POT1, leading to chromosome aberrations such as telomere fusions and telomere doublets. Analysis of the molecular damage pathway revealed that RHPS4 induced an ATR-dependent ATM signaling that plays a functional role in the cellular response to RHPS4 treatment. We propose that RHPS4, by stabilizing G4 DNA at telomeres, impairs fork progression and/or telomere processing resulting in telomere dysfunction and activation of a replication stress response pathway. The detailed understanding of the molecular mode of action of this class of compounds makes them attractive tools to understand telomere biology and provides the basis for a rational use of G4 ligands for the therapy of cancer.
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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.