ReviewJournal of molecular cell biology2011
More forks on the road to replication stress recovery.
Review in Journal of molecular cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Inherited variation at chromosome 12p13.33, including RAD52, influences the risk of squamous cell lung carcinoma.Cancer discovery · 2012Pooled it
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023Review
- Epigenetic upregulation of Schlafen11 renders WNT- and SHH-activated medulloblastomas sensitive to cisplatin.Neuro-oncology · 2023Article
- Roles of homologous recombination in response to ionizing radiation-induced DNA damage.International journal of radiation biology · 2023Review
- Accumulation of DNA damage alters microRNA gene transcription in Arabidopsis thaliana.BMC plant biology · 2022Article
- Targeting NPM1 in irradiated cells inhibits NPM1 binding to RAD51, RAD51 foci formation and radiosensitizes NSCLC.Cancer letters · 2021Article
- Exploiting DNA repair pathways for tumor sensitization, mitigation of resistance, and normal tissue protection in radiotherapy.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Genetic Interaction Between Site-Specific Epigenetic Marks and Roles of H4v in Transcription Termination inFrontiers in cell and developmental biology · 2021Article
- Review
- Distinct roles of structure-specific endonucleases EEPD1 and Metnase in replication stress responses.NAR cancer · 2020Article
- Clustered DNA Double-Strand Breaks: Biological Effects and Relevance to Cancer Radiotherapy.Genes · 2020Review
- DNA-PKcs: A Multi-Faceted Player in DNA Damage Response.Frontiers in genetics · 2020Review
- Checkpoint inhibition of origin firing prevents DNA topological stress.Genes & development · 2019Article
- MiR223-3p promotes synthetic lethality in BRCA1-deficient cancers.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- RECQL5 plays an essential role in maintaining genome stability and viability of triple-negative breast cancer cells.Cancer medicine · 2019Article
- DNA Repair Gene Expression Adjusted by theCancers · 2019Article
- Small Molecule Docking of DNA Repair Proteins Associated with Cancer Survival Following PCNA Metagene Adjustment: A Potential Novel Class of Repair Inhibitors.Molecules (Basel, Switzerland) · 2019Article
- Genome-wide function of MCM-BP in Trypanosoma brucei DNA replication and transcription.Nucleic acids research · 2019Article
- Evaluating the role of RAD52 and its interactors as novel potential molecular targets for hepatocellular carcinoma.Cancer cell international · 2019Article
28 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
High-fidelity replication of DNA, and its accurate segregation to daughter cells, is critical for maintaining genome stability and suppressing cancer. DNA replication forks are stalled by many DNA lesions, activating checkpoint proteins that stabilize stalled forks. Stalled forks may eventually collapse, producing a broken DNA end. Fork restart is typically mediated by proteins initially identified by their roles in homologous recombination repair of DNA double-strand breaks (DSBs). In recent years, several proteins involved in DSB repair by non-homologous end joining (NHEJ) have been implicated in the replication stress response, including DNA-PKcs, Ku, DNA Ligase IV-XRCC4, Artemis, XLF and Metnase. It is currently unclear whether NHEJ proteins are involved in the replication stress response through indirect (signaling) roles, and/or direct roles involving DNA end joining. Additional complexity in the replication stress response centers around RPA, which undergoes significant post-translational modification after stress, and RAD52, a conserved HR protein whose role in DSB repair may have shifted to another protein in higher eukaryotes, such as BRCA2, but retained its role in fork restart. Most cancer therapeutic strategies create DNA replication stress. Thus, it is imperative to gain a better understanding of replication stress response proteins and pathways to improve cancer therapy.
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.