ArticleNucleic acids research2016
PrimPol prevents APOBEC/AID family mediated DNA mutagenesis.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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
34 citing papers in PubMed, 65 citations in OpenAlex.
- Targeting common denominators of DNA damage tolerance mechanisms as therapeutic strategy to cope with dynamic phenotypic changes in triple-negative breast cancer cells.Cell death discovery · 2026Article
- Mesenchymal stem cell derived extracellular vesicles reverses neural aging via OSKM modulation.Cell communication and signaling : CCS · 2025Article
- Replication stress responses in human lymphocytes change sex-specifically during aging.Nucleic acids research · 2025Article
- Archaeal replicative primase mediates DNA double-strand break repair.Nucleic acids research · 2025Article
- Molecular dependencies and genomic consequences of a global DNA damage tolerance defect.Genome biology · 2024Article
- Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation.Science China. Life sciences · 2024Review
- Review
- The SMC5/6 complex prevents genotoxicity upon APOBEC3A-mediated replication stress.The EMBO journal · 2024Article
- APOBEC3A induces DNA gaps through PRIMPOL and confers gap-associated therapeutic vulnerability.Science advances · 2024Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- Multi-omics analysis of DNA replication-associated primase polymerase (PRIMPOL) in pan-cancer: a potential target for prognosis and immune response.European journal of medical research · 2023Article
- Article
- PrimPol: A Breakthrough among DNA Replication Enzymes and a Potential New Target for Cancer Therapy.Biomolecules · 2022Review
- PARP Inhibition and Beyond in BRCA-Associated Breast Cancer in Women: A State-Of-The-Art Summary of Preclinical Research on Risk Reduction and Clinical Benefits.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2022Review
- REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps.Molecular cell · 2021Article
- Repriming DNA synthesis: an intrinsic restart pathway that maintains efficient genome replication.Nucleic acids research · 2021Review
- Translesion Synthesis or Repair by Specialized DNA Polymerases Limits Excessive Genomic Instability upon Replication Stress.International journal of molecular sciences · 2021Review
- PRIMPOL ready, set, reprime!Critical reviews in biochemistry and molecular biology · 2021Review
- HLTF Promotes Fork Reversal, Limiting Replication Stress Resistance and Preventing Multiple Mechanisms of Unrestrained DNA Synthesis.Molecular cell · 2020Article
- Identifying the role of PrimPol in TDF-induced toxicity and implications of its loss of function mutation in an HIV+ patient.Scientific reports · 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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PrimPol is a DNA damage tolerant polymerase displaying both translesion synthesis (TLS) and (re)-priming properties. This led us to study the consequences of a PrimPol deficiency in tolerating mutagenic lesions induced by members of the APOBEC/AID family of cytosine deaminases. Interestingly, during somatic hypermutation, PrimPol counteracts the generation of C>G transversions on the leading strand. Independently, mutation analyses in human invasive breast cancer confirmed a pro-mutagenic activity of APOBEC3B and revealed a genome-wide anti-mutagenic activity of PRIMPOL as well as most Y-family TLS polymerases. PRIMPOL especially prevents APOBEC3B targeted cytosine mutations within TpC dinucleotides. As C transversions induced by APOBEC/AID family members depend on the formation of AP-sites, we propose that PrimPol reprimes preferentially downstream of AP-sites on the leading strand, to prohibit error-prone TLS and simultaneously stimulate error-free homology directed repair. These in vivo studies are the first demonstrating a critical anti-mutagenic activity of PrimPol in genome maintenance.
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.