ArticleCell cycle (Georgetown, Tex.)2016
PrimPol-deficient cells exhibit a pronounced G2 checkpoint response following UV damage.
Article in Cell cycle (Georgetown, Tex.), 2016. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Archaeal replicative primase mediates DNA double-strand break repair.Nucleic acids research · 2025Article
- RNA Sequencing and Bioinformatics Analysis Reveals the Downregulation of DNA Replication Genes by Morindone in Colorectal Cancer Cells.Applied biochemistry and biotechnology · 2024Article
- The role of catalytic and regulatory domains of human PrimPol in DNA binding and synthesis.Nucleic acids research · 2023Article
- PLK1 regulates the PrimPol damage tolerance pathway during the cell cycle.Science advances · 2021Article
- Arabidopsis thaliana PrimPol is a primase and lesion bypass DNA polymerase with the biochemical characteristics to cope with DNA damage in the nucleus, mitochondria, and chloroplast.Scientific reports · 2021Article
- BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage.Nature communications · 2021Article
- Repriming DNA synthesis: an intrinsic restart pathway that maintains efficient genome replication.Nucleic acids research · 2021Review
- Mechanisms for Maintaining Eukaryotic Replisome Progression in the Presence of DNA Damage.Frontiers in molecular biosciences · 2021Review
- The deubiquitinase USP36 Regulates DNA replication stress and confers therapeutic resistance through PrimPol stabilization.Nucleic acids research · 2020Article
- Structure-Function Analysis Reveals the Singularity of Plant Mitochondrial DNA Replication Components: A Mosaic and Redundant System.Plants (Basel, Switzerland) · 2019Review
- PrimPol is required for the maintenance of efficient nuclear and mitochondrial DNA replication in human cells.Nucleic acids research · 2019Article
- Comparative genomics sheds light on the predatory lifestyle of accipitrids and owls.Scientific reports · 2019Article
- G4-Interacting DNA Helicases and Polymerases: Potential Therapeutic Targets.Current medicinal chemistry · 2019Review
- PrimPol is required for replication reinitiation after mtDNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- DNA Damage Tolerance by Eukaryotic DNA Polymerase and Primase PrimPol.International journal of molecular sciences · 2017Review
- Mitochondrial DNA replication: a PrimPol perspective.Biochemical Society transactions · 2017Review
- PrimPol-Prime Time to Reprime.Genes · 2017Review
- Repriming by PrimPol is critical for DNA replication restart downstream of lesions and chain-terminating nucleosides.Cell cycle (Georgetown, Tex.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
PrimPol is a recently identified member of the archaeo-eukaryote primase (AEP) family of primase-polymerases. It has been shown that this mitochondrial and nuclear localized enzyme plays roles in the maintenance of both unperturbed replication fork progression and in the bypass of lesions after DNA damage. Here, we utilized an avian (DT40) knockout cell line to further study the consequences of loss of PrimPol (PrimPol(-/-)) on the downstream maintenance of cells after UV damage. We report that PrimPol(-/-) cells are more sensitive to UV-C irradiation in colony survival assays than Pol η-deficient cells. Although this increased UV sensitivity is not evident in cell viability assays, we show that this discrepancy is due to an enhanced checkpoint arrest after UV-C damage in the absence of PrimPol. PrimPol(-/-) arrested cells become stalled in G2, where they are protected from UV-induced cell death. Despite lacking an enzyme required for the bypass and maintenance of replication fork progression in the presence of UV damage, we show that PrimPol(-/-) cells actually have an advantage in the presence of a Chk1 inhibitor due to their slow progression through S-phase.
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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.