Evidence map›Paper›PMID 28180309›Full record

ArticleNucleic acids research2017

Predominant role of DNA polymerase eta and p53-dependent translesion synthesis in the survival of ultraviolet-irradiated human cells.

Leticia K Lerner, Guilherme Francisco, Daniela T Soltys, Clarissa R R Rocha, Annabel Quinet, Alexandre T Vessoni, Ligia P Castro, Taynah I P David, Silvina O Bustos, Bryan E Strauss and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Translesion Synthesis DNA Polymerase Gene Expression Is Impacted by Age and IGF-1 in Epidermal Human Skin.JID innovations : skin science from molecules to population health · 2025
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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

15 authors at 5 institutions in 3 countries.

Leticia K LernerDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Guilherme FranciscoDepartment of Center for Translational Oncology Cellular, Biology Group, Center for Translational Oncology, Cancer Institute of the State of São Paulo-ICESP, São Paulo, Brazil.
Daniela T SoltysDepartment of Biochemistry, Institute of Chemistry, University of São Paulo, São Paulo, Brazil.
Clarissa R R RochaDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Annabel QuinetDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Alexandre T VessoniDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Ligia P CastroDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Taynah I P DavidViral Vector Laboratory, Heart Institute, University of São Paulo, São Paulo, Brazil.
Silvina O BustosDepartment of Center for Translational Oncology Cellular, Biology Group, Center for Translational Oncology, Cancer Institute of the State of São Paulo-ICESP, São Paulo, Brazil.
Bryan E StraussViral Vector Laboratory, Heart Institute, University of São Paulo, São Paulo, Brazil.
Vanesa GottifrediCell Cycle and Genomic Stability Laboratory, Fundación Instituto Leloir-CONICET, Buenos Aires, Argentina.
Anne StaryCNRS-UMR8200, Université Paris-Sud, Institut de Cancérologie Gustave Roussy, Villejuif, France.
Alain SarasinCNRS-UMR8200, Université Paris-Sud, Institut de Cancérologie Gustave Roussy, Villejuif, France.
Roger ChammasDepartment of Center for Translational Oncology Cellular, Biology Group, Center for Translational Oncology, Cancer Institute of the State of São Paulo-ICESP, São Paulo, Brazil.
Carlos F M MenckDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Universidade de São Paulo · BRInstituto do Câncer do Estado de São Paulo · BRCentre National de la Recherche Scientifique · FRConsejo Nacional de Investigaciones Científicas y Técnicas · ARInstitut Gustave Roussy · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome lesions trigger biological responses that help cells manage damaged DNA, improving cell survival. Pol eta is a translesion synthesis (TLS) polymerase that bypasses lesions that block replicative polymerases, avoiding continued stalling of replication forks, which could lead to cell death. p53 also plays an important role in preventing cell death after ultraviolet (UV) light exposure. Intriguingly, we show that p53 does so by favoring translesion DNA synthesis by pol eta. In fact, the p53-dependent induction of pol eta in normal and DNA repair-deficient XP-C human cells after UV exposure has a protective effect on cell survival after challenging UV exposures, which was absent in p53- and Pol H-silenced cells. Viability increase was associated with improved elongation of nascent DNA, indicating the protective effect was due to more efficient lesion bypass by pol eta. This protection was observed in cells proficient or deficient in nucleotide excision repair, suggesting that, from a cell survival perspective, proper bypass of DNA damage can be as relevant as removal. These results indicate p53 controls the induction of pol eta in DNA damaged human cells, resulting in improved TLS and enhancing cell tolerance to DNA damage, which parallels SOS responses in bacteria.

Indexed as

Cell LineCell SurvivalChromatinDNADNA-Directed DNA PolymeraseDNA RepairDNA ReplicationDose-Response Relationship, RadiationFibroblastsGene Expression RegulationHumansTumor Suppressor Protein p53Ultraviolet RaysY-Family DNA PolymerasesChromatinDNADNA-Directed DNA PolymeraseRad30 proteinTP53 protein, humanTumor Suppressor Protein p53Y-Family DNA Polymerases

Identifiers

PMID28180309
PMCPMC5388406
OpenAlexW2559912224

What OpenQuestion holds

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LicenceCC BY-NC
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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.