ArticleCell stress2017
A game of substrates: replication fork remodeling and its roles in genome stability and chemo-resistance.
Article in Cell stress, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Site-saturation functional screens identify PALB2 missense variants associated with increased breast cancer risk.Nature communications · 2026Article
- Potential Resistance to Oxaliplatin-Based Regimens in Gastric Cancer Patients with ERBB2 R678Q Mutation: Evidence from a National Genomic Database.Current issues in molecular biology · 2025Article
- APLF facilitates interstrand DNA crosslink repair and replication fork protection to confer cisplatin resistance.Nucleic acids research · 2024Article
- Multifaceted Role of PARP1 in Maintaining Genome Stability Through Its Binding to Alternative DNA Structures.Journal of molecular biology · 2024Review
- WRN helicase safeguards deprotected replication forks in BRCA2-mutated cancer cells.Nature communications · 2021Article
- Mind the replication gap.Royal Society open science · 2021Review
- DCAF14 promotes stalled fork stability to maintain genome integrity.Cell reports · 2021Article
- DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells.Experimental & molecular medicine · 2020Review
- Deoxyuracil in DNA in health and disease.Current opinion in clinical nutrition and metabolic care · 2020Review
- E3 ligase RFWD3 is a novel modulator of stalled fork stability in BRCA2-deficient cells.The Journal of cell biology · 2020Article
- Functional Characterization ofFrontiers in molecular biosciences · 2020Review
- Replication Fork Remodeling and Therapy Escape in DNA Damage Response-Deficient Cancers.Frontiers in oncology · 2020Review
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- Article
- Fine-tuning of the replisome: Mcm10 regulates fork progression and regression.Cell cycle (Georgetown, Tex.) · 2019Review
- Review
- Mcm10 has potent strand-annealing activity and limits translocase-mediated fork regression.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Loss of Cohesin Subunit Rec8 Switches Rad51 Mediator Dependence in Resistance to Formaldehyde Toxicity inGenetics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
During the hours that human cells spend in the DNA synthesis (S) phase of the cell cycle, they may encounter adversities such as DNA damage or shortage of nucleotides. Under these stresses, replication forks in DNA may experience slowing, stalling, and breakage. Fork remodeling mechanisms, which stabilize slow or stalled replication forks and ensure their ability to continue or resume replication, protect cells from genomic instability and carcinogenesis. Fork remodeling includes DNA strand exchanges that result in annealing of newly synthesized strands (fork reversal), controlled DNA resection, and cleavage of DNA strands. Defects in major tumor suppressor genes BRCA1 and BRCA2, and a subset of the Fanconi Anemia genes have been shown to result in deregulation in fork remodeling, and most prominently, loss of kilobases of nascent DNA from stalled replication forks. This phenomenon has recently gained spotlight as a potential marker and mediator of chemo-sensitivity in cancer cells and, conversely, its suppression - as a hallmark of acquired chemo-resistance. Moreover, nascent strand degradation at forks is now known to also trigger innate immune response to self-DNA. An increasingly sophisticated molecular description of these events now points at a combination of unbalanced fork reversal and end-resection as a root cause, yet also reveals the multi-layered complexity and heterogeneity of the underlying processes in normal and cancer cells.
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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.