Evidence map›Paper›PMID 24240614›Full record

ArticleNature structural & molecular biology2013

Repriming of DNA synthesis at stalled replication forks by human PrimPol.

Silvana Mourón, Sara Rodriguez-Acebes, María I Martínez-Jiménez, Sara García-Gómez, Sandra Chocrón, Luis Blanco, Juan Méndez

Abstract read
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In one paragraph

Article in Nature structural & molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 1 synthesis or guideline pooled it, 317 citations in OpenAlex.

  1. Pooled it
  2. Quiescence to proliferation transition regulates asynchronous mitochondrial DNA replication dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026
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158 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Silvana MourónMolecular Oncology Program, Spanish National Cancer Research Centre, Madrid, Spain.
Sara Rodriguez-Acebes
María I Martínez-Jiménez
Sara García-Gómez
Sandra Chocrón
Luis Blanco
Juan Méndez
Centro de Biología Molecular Severo Ochoa · ESSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA replication forks that collapse during the process of genomic duplication lead to double-strand breaks and constitute a threat to genomic stability. The risk of fork collapse is higher in the presence of replication inhibitors or after UV irradiation, which introduces specific modifications in the structure of DNA. In these cases, fork progression may be facilitated by error-prone translesion synthesis (TLS) DNA polymerases. Alternatively, the replisome may skip the damaged DNA, leaving an unreplicated gap to be repaired after replication. This mechanism strictly requires a priming event downstream of the lesion. Here we show that PrimPol, a new human primase and TLS polymerase, uses its primase activity to mediate uninterrupted fork progression after UV irradiation and to reinitiate DNA synthesis after dNTP depletion. As an enzyme involved in tolerance to DNA damage, PrimPol might become a target for cancer therapy.

Indexed as

DNA Breaks, Double-StrandedDNA DamageDNA-Directed DNA PolymeraseDNA PrimaseDNA ReplicationGenomic InstabilityHumansMultifunctional EnzymesRNA, MessengerS PhaseUltraviolet RaysDNA-Directed DNA PolymeraseDNA PrimaseMultifunctional EnzymesPrimPol protein, humanRNA, Messenger

Identifiers

PMID24240614
OpenAlexW2038185005

What OpenQuestion holds

Textmetadata
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.