ArticleNucleic acids research2014
Persistently stalled replication forks inhibit nucleotide excision repair in trans by sequestering Replication protein A.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- REV1 Loss Triggers a G2/M Cell-Cycle Arrest Through Dysregulation of Mitotic Regulators.Genes · 2025Article
- Schedule-Dependent Treatment Increases Chemotherapy Efficacy in Malignant Pleural Mesothelioma.International journal of molecular sciences · 2022Article
- A genome-wide screen identifies SCAI as a modulator of the UV-induced replicative stress response.PLoS biology · 2022Article
- TREX1 degrades the 3' end of the small DNA oligonucleotide products of nucleotide excision repair in human cells.Nucleic acids research · 2022Article
- REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis.Cell death & disease · 2022Article
- Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins.Genetics and molecular biology · 2020Article
- DNA damage tolerance in stem cells, ageing, mutagenesis, disease and cancer therapy.Nucleic acids research · 2019Review
- Occurrence of acute myeloid leukemia in hydroxyurea-treated sickle cell disease patient.Cancer biology & therapy · 2019Article
- Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.Environmental and molecular mutagenesis · 2018Review
- Impact of Age and Insulin-Like Growth Factor-1 on DNA Damage Responses in UV-Irradiated Human Skin.Molecules (Basel, Switzerland) · 2017Review
- Insulin-like Growth Factor 1 Receptor Signaling Is Required for Optimal ATR-CHK1 Kinase Signaling in Ultraviolet B (UVB)-irradiated Human Keratinocytes.The Journal of biological chemistry · 2017Article
- Article
- Mutations in Replicative Stress Response Pathways Are Associated with S Phase-specific Defects in Nucleotide Excision Repair.The Journal of biological chemistry · 2016Article
- Oxidative Damage to RPA Limits the Nucleotide Excision Repair Capacity of Human Cells.The Journal of investigative dermatology · 2015Article
- Replication protein A prevents promiscuous annealing between short sequence homologies: Implications for genome integrity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rev3, the catalytic subunit of DNA polymerase ζ, is essential for translesion synthesis of cytotoxic DNA photolesions, whereas the Rev1 protein plays a noncatalytic role in translesion synthesis. Here, we reveal that mammalian Rev3(-/-) and Rev1(-/-) cell lines additionally display a nucleotide excision repair (NER) defect, specifically during S phase. This defect is correlated with the normal recruitment but protracted persistence at DNA damage sites of factors involved in an early stage of NER, while repair synthesis is affected. Remarkably, the NER defect becomes apparent only at 2 h post-irradiation indicating that Rev3 affects repair synthesis only indirectly, rather than performing an enzymatic role in NER. We provide evidence that the NER defect is caused by scarceness of Replication protein A (Rpa) available to NER, resulting from its sequestration at stalled replication forks. Also the induction of replicative stress using hydroxyurea precludes the accumulation of Rpa at photolesion sites, both in Rev3(-/-) and in wild-type cells. These data support a model in which the limited Rpa pool coordinates replicative stress and NER, resulting in increased cytotoxicity of ultraviolet light when replicative stress exceeds a threshold.
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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.