ArticleMolecular cell2018
Genome-wide Identification of Structure-Forming Repeats as Principal Sites of Fork Collapse upon ATR Inhibition.
Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
56 citing papers in PubMed, 82 citations in OpenAlex.
- Genome-wide mapping of replication stress response factors reveals the management of polycistronic transcription, replication initiation, and responses to replication stress in Leishmania.Nucleic acids research · 2026Article
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- TONSOKU prevents the formation of large tandem duplications and restrains ATR-WEE1 checkpoint activation.Nature communications · 2026Article
- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 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
- Computational tools for tandem repeat detection using long-read sequencing.Briefings in bioinformatics · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- TRsv: simultaneous detection of tandem repeat variations, structural variations, and short indels using long read sequencing data.Genome biology · 2025Article
- ThebioRxiv : the preprint server for biology · 2025Article
- Replicative DNA polymerase epsilon and delta holoenzymes show wide-ranging inhibition at G-quadruplexes in the human genome.Nucleic acids research · 2025Article
- DNA polymerase zeta can efficiently replicate structures formed by AT/TA repeat sequences and prevent their deletion.Nucleic acids research · 2025Article
- Precise Mapping of Physiological DSBs Using In-Suspension Break Labeling In Situ and Sequencing (sBLISS).Methods in molecular biology (Clifton, N.J.) · 2025Article
- Ni(II) Cylinders Damage DNA in Cancer Cells and Preferentially Bind Y-Shaped DNA Three-Way Junctions Blocking DNA Synthesis.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- Article
- Somatic and intergenerational G4C2 hexanucleotide repeat instability in a human C9orf72 knock-in mouse model.Nucleic acids research · 2024Article
- Improved detection of DNA replication fork-associated proteins.Cell reports · 2024Article
- DNA Damage Atlas: an atlas of DNA damage and repair.Nucleic acids research · 2024Article
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Replication-induced DNA secondary structures drive fork uncoupling and breakage.The EMBO journal · 2023Article
Corrections and comments
- Commented on by
Authors and funding
23 authors at 7 institutions in 1 country.
Funding
Abstract
DNA polymerase stalling activates the ATR checkpoint kinase, which in turn suppresses fork collapse and breakage. Herein, we describe use of ATR inhibition (ATRi) as a means to identify genomic sites of problematic DNA replication in murine and human cells. Over 500 high-resolution ATR-dependent sites were ascertained using two distinct methods: replication protein A (RPA)-chromatin immunoprecipitation (ChIP) and breaks identified by TdT labeling (BrITL). The genomic feature most strongly associated with ATR dependence was repetitive DNA that exhibited high structure-forming potential. Repeats most reliant on ATR for stability included structure-forming microsatellites, inverted retroelement repeats, and quasi-palindromic AT-rich repeats. Notably, these distinct categories of repeats differed in the structures they formed and their ability to stimulate RPA accumulation and breakage, implying that the causes and character of replication fork collapse under ATR inhibition can vary in a DNA-structure-specific manner. Collectively, these studies identify key sources of endogenous replication stress that rely on ATR for stability.
Indexed as
Identifiers
What OpenQuestion holds
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.