ArticleThe Journal of biological chemistry2012
Replication fork stalling and checkpoint activation by a PKD1 locus mirror repeat polypurine-polypyrimidine (Pu-Py) tract.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 46 citations in OpenAlex.
- A new conceptual framework for PKD1 in ADPKD; integrating DNA structures and inflammation.BMC nephrology · 2026Review
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- G-quadruplex stabilization provokes DNA breaks in human PKD1, revealing a second hit mechanism for ADPKD.Nature communications · 2025Article
- Somatic mutation in autosomal dominant polycystic kidney disease revealed by deep sequencing human kidney cysts.NPJ genomic medicine · 2024Article
- Triplex H-DNA structure: the long and winding road from the discovery to its role in human disease.NAR molecular medicine · 2024Article
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- Pathogenic CANVAS (AAGGG)n repeats stall DNA replication due to the formation of alternative DNA structures.Nucleic acids research · 2024Article
- HumanmicroPublication biology · 2024Article
- Article
- S1-END-seq reveals DNA secondary structures in human cells.Molecular cell · 2022Article
- Stable G-quadruplex DNA structures promote replication-dependent genome instability.The Journal of biological chemistry · 2022Article
- Non-canonical DNA structures: Diversity and disease association.Frontiers in genetics · 2022Review
- Translesion polymerase eta both facilitates DNA replication and promotes increased human genetic variation at common fragile sites.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Sweet Melody or Jazz? Transcription Around DNA Double-Strand Breaks.Frontiers in molecular biosciences · 2021Review
- Human CTC1 promotes TopBP1 stability and CHK1 phosphorylation in response to telomere dysfunction and global replication stress.Cell cycle (Georgetown, Tex.) · 2020Article
- Replication stress at microsatellites causes DNA double-strand breaks and break-induced replication.The Journal of biological chemistry · 2020Article
- Timeless couples G-quadruplex detection with processing by DDX11 helicase during DNA replication.The EMBO journal · 2020Article
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Detection and characterization of mosaicism in autosomal dominant polycystic kidney disease.Kidney international · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
DNA sequences prone to forming noncanonical structures (hairpins, triplexes, G-quadruplexes) cause DNA replication fork stalling, activate DNA damage responses, and represent hotspots of genomic instability associated with human disease. The 88-bp asymmetric polypurine-polypyrimidine (Pu-Py) mirror repeat tract from the human polycystic kidney disease (PKD1) intron 21 forms non-B DNA secondary structures in vitro. We show that the PKD1 mirror repeat also causes orientation-dependent fork stalling during replication in vitro and in vivo. When integrated alongside the c-myc replicator at an ectopic chromosomal site in the HeLa genome, the Pu-Py mirror repeat tract elicits a polar replication fork barrier. Increased replication protein A (RPA), Rad9, and ataxia telangiectasia- and Rad3-related (ATR) checkpoint protein binding near the mirror repeat sequence suggests that the DNA damage response is activated upon replication fork stalling. Moreover, the proximal c-myc origin of replication was not required to cause orientation-dependent checkpoint activation. Cells expressing the replication fork barrier display constitutive Chk1 phosphorylation and continued growth, i.e. checkpoint adaptation. Excision of the Pu-Py mirror repeat tract abrogates the DNA damage response. Adaptation to Chk1 phosphorylation in cells expressing the replication fork barrier may allow the accumulation of mutations that would otherwise be remediated by the DNA damage response.
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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.