Evidence map›Paper›PMID 23761444›Full record

ArticleNucleic acids research2013

DNA-damage tolerance mediated by PCNA*Ub fusions in human cells is dependent on Rev1 but not Polη.

Zhoushuai Qin, Mengxue Lu, Xin Xu, Michelle Hanna, Naoko Shiomi, Wei Xiao

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Beyond the Lesion: Back to High Fidelity DNA Synthesis.Frontiers in molecular biosciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Zhoushuai QinCollege of Life Sciences, Capital Normal University, Beijing 100048, China, Department of Microbiology and Immunology, University of Saskatchewan, Saskatoon S7N 5E5, Canada and Project for Environmental Dynamics and Radiation Effects, Fukushima Project Headquarters, National Institute of Radiological Sciences, Chiba 263-8555, Japan.
Mengxue Lu
Xin Xu
Michelle Hanna
Naoko Shiomi
Wei Xiao
National Institutes for Quantum and Radiological Science and Technology · JPCapital Normal University · CNUniversity of Saskatchewan · CA

Funding

Canadian Institutes of Health Research MOP-93612
6 · The paper itself

Abstract

In response to replication-blocking lesions, proliferating cell nuclear antigen (PCNA) can be sequentially ubiquitinated at the K164 residue, leading to two modes of DNA-damage tolerance, namely, translesion DNA synthesis (TLS) and error-free lesion bypass. Although the majority of reported data support a model whereby monoubiquitinated PCNA enhances its affinity for TLS polymerases and hence recruits them to the damage sites, this model has also been challenged by several observations. In this study, we expressed the PCNA-164R and ubiquitin (UB) fusion genes in an inducible manner in an attempt to mimic PCNA monoubiquitination in cultured human cells. It was found that expression of both N- and C-terminal PCNA•Ub fusions conferred significant tolerance to ultraviolet (UV)-induced DNA damage. Surprisingly, depletion of Polη, a TLS polymerase dedicated to bypassing UV-induced pyrimidine dimers, did not alter tolerance conferred by PCNA•Ub. In contrast, depletion of Rev1, another TLS polymerase serving as a scaffold for the assembly of the TLS complex, completely abolished PCNA•Ub-mediated damage tolerance. Similar genetic interactions were confirmed when UV-induced monoubiquitination of endogenous PCNA is abolished by RAD18 deletion. Hence, PCNA•Ub fusions bypass the requirement for PCNA monoubiquitination, and UV damage tolerance conferred by these fusions is dependent on Rev1 but independent of Polη.

Indexed as

ChromatinDNA-Binding ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA ReplicationEpistasis, GeneticGene FusionHCT116 CellsHEK293 CellsHumansMutationNuclear ProteinsNucleotidyltransferasesProliferating Cell Nuclear AntigenPyrimidine DimersSaccharomyces cerevisiaeChromatinDNA-Binding ProteinsDNA-Directed DNA PolymeraseNuclear ProteinsNucleotidyltransferasesProliferating Cell Nuclear AntigenPyrimidine DimersRAD18 protein, humanREV1 protein, humanUbiquitinUbiquitin-Protein LigasesY-Family DNA Polymerases

Identifiers

PMID23761444
PMCPMC3753651
OpenAlexW2017372213

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.