ArticleeLife2016
Characterization of human translesion DNA synthesis across a UV-induced DNA lesion.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- smDeepFLUOR: single-molecule deep learning fluorescence classification.Nature communications · 2026Article
- PCNA encircling primer/template junctions is eliminated by exchange of RPA for Rad51: implications for the interplay between human DNA damage tolerance pathways.Nucleic acids research · 2026Article
- Therapeutic 6-thio-deoxyguanosine inhibits telomere elongation in cancer cells by inducing a non-productive stalled telomerase complex.Nature communications · 2025Article
- Residues in the little finger domain of the Y-family Dpo4 DNA polymerase communicate to restrict synthesis past 8-oxoguanine lesions.Nucleic acids research · 2025Article
- Replication protein A dynamically re-organizes on primer/template junctions to permit DNA polymerase δ holoenzyme assembly and initiation of DNA synthesis.Nucleic acids research · 2024Article
- Tracking of progressing human DNA polymerase δ holoenzymes reveals distributions of DNA lesion bypass activities.Nucleic acids research · 2022Article
- Determination of DNA lesion bypass using a ChIP-based assay.DNA repair · 2021Article
- Cryo-EM structure of human Pol κ bound to DNA and mono-ubiquitylated PCNA.Nature communications · 2021Article
- Beyond the Lesion: Back to High Fidelity DNA Synthesis.Frontiers in molecular biosciences · 2021Review
- Focus on UV-Induced DNA Damage and Repair-Disease Relevance and Protective Strategies.International journal of molecular sciences · 2020Review
- DUSP3 maintains genomic stability and cell proliferation by modulating NER pathway and cell cycle regulatory proteins.Cell cycle (Georgetown, Tex.) · 2020Article
- Human PCNA Structure, Function and Interactions.Biomolecules · 2020Review
- Structure of the processive human Pol δ holoenzyme.Nature communications · 2020Article
- Structural insights into mutagenicity of anticancer nucleoside analog cytarabine during replication by DNA polymerase η.Scientific reports · 2019Article
- The p12 subunit of human polymerase δ uses an atypical PIP box for molecular recognition of proliferating cell nuclear antigen (PCNA).The Journal of biological chemistry · 2019Article
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
- p15PAF binding to PCNA modulates the DNA sliding surface.Nucleic acids research · 2018Article
- Phosphorylation Alters the Properties of Pol η: Implications for Translesion Synthesis.iScience · 2018Article
- Review
- Lesion Bypass and the Reactivation of Stalled Replication Forks.Annual review of biochemistry · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Translesion DNA synthesis (TLS) during S-phase uses specialized TLS DNA polymerases to replicate a DNA lesion, allowing stringent DNA synthesis to resume beyond the offending damage. Human TLS involves the conjugation of ubiquitin to PCNA clamps encircling damaged DNA and the role of this post-translational modification is under scrutiny. A widely-accepted model purports that ubiquitinated PCNA recruits TLS polymerases such as pol η to sites of DNA damage where they may also displace a blocked replicative polymerase. We provide extensive quantitative evidence that the binding of pol η to PCNA and the ensuing TLS are both independent of PCNA ubiquitination. Rather, the unique properties of pols η and δ are attuned to promote an efficient and passive exchange of polymerases during TLS on the lagging strand.
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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.