ArticleNucleic acids research2016
Triplex structures induce DNA double strand breaks via replication fork collapse in NER deficient cells.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 43 citations in OpenAlex.
- Highly Potent Fluorogenic Ligands for Triplex DNA: 5-Substituted 2-(Naphthalen-2-yl)-4H-Chromen-4-Ones.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- HSeeker: an algorithm for systematic H-DNA sequence identification.bioRxiv : the preprint server for biology · 2026Article
- Alternative nucleic acid structures in microbial biology: regulatory functions and antimicrobial opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Cell-penetrating antibody enhances nuclear delivery of triplex-forming oligonucleotides targeting HER2-positive cancers.Molecular therapy. Nucleic acids · 2025Article
- Efficacy of DNA Intercalator-Conjugated Triplex-Forming Oligonucleotide as Anticancer Agent.ChemMedChem · 2025Article
- Development and functional evaluation of a psoralen-conjugated nucleoside mimic for triplex-forming oligonucleotides.Communications chemistry · 2025Article
- Elucidating the Role of Groove Hydration on Stability and Functions of Biased DNA Duplexes in Cell-Like Chemical Environments.Journal of the American Chemical Society · 2024Article
- The molecular mechanism for TERRA recruitment and annealing to telomeres.Nucleic acids research · 2024Article
- TTSBBC: triplex target site biomarkers and barcodes in cancer.Nucleic acids research · 2024Article
- Understanding intercalative modulation of G-rich sequence folding: solution structure of a TINA-conjugated antiparallel DNA triplex.Nucleic acids research · 2024Article
- The Development of Non-natural Type Nucleoside to Stabilize Triplex DNA Formation against CG and TA Inversion Site.Current medicinal chemistry · 2024Review
- Recent Advancements in Development and Therapeutic Applications of Genome-Targeting Triplex-Forming Oligonucleotides and Peptide Nucleic Acids.Pharmaceutics · 2023Review
- Inhibition of transcription and antiproliferative effects in a cancer cell line using antigene oligonucleotides containing artificial nucleoside analogues.RSC medicinal chemistry · 2023Article
- Structural underpinnings of mutation rate variations in the human genome.Nucleic acids research · 2023Article
- SOX10 modulated SMARCA4 dysregulation alleviates DNA replication stress in cutaneous melanoma.Journal of cellular and molecular medicine · 2022Article
- Characterization of somatic structural variations in 528 Chinese individuals with Esophageal squamous cell carcinoma.Nature communications · 2022Article
- Switching G-quadruplex to parallel duplex by molecular rotor clustering.Nucleic acids research · 2022Article
- TRF2 recruits nucleolar protein TCOF1 to coordinate telomere transcription and replication.Cell death and differentiation · 2021Article
- Article
- Small Circular DNA Molecules as Triangular Scaffolds for the Growth of 3D Single Crystals.Biomolecules · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Structural alterations in DNA can serve as natural impediments to replication fork stability and progression, resulting in DNA damage and genomic instability. Naturally occurring polypurine mirror repeat sequences in the human genome can create endogenous triplex structures evoking a robust DNA damage response. Failures to recognize or adequately process these genomic lesions can result in loss of genomic integrity. Nucleotide excision repair (NER) proteins have been found to play a prominent role in the recognition and repair of triplex structures. We demonstrate using triplex-forming oligonucleotides that chromosomal triplexes perturb DNA replication fork progression, eventually resulting in fork collapse and the induction of double strand breaks (DSBs). We find that cells deficient in the NER damage recognition proteins, XPA and XPC, accumulate more DSBs in response to chromosomal triplex formation than NER-proficient cells. Furthermore, we demonstrate that XPC-deficient cells are particularly prone to replication-associated DSBs in the presence of triplexes. In the absence of XPA or XPC, deleterious consequences of triplex-induced genomic instability may be averted by activating apoptosis via dual phosphorylation of the H2AX protein. Our results reveal that damage recognition by XPC and XPA is critical to maintaining replication fork integrity and preventing replication fork collapse in the presence of triplex structures.
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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.