Evidence map›Paper›PMID 34128550›Full record

ArticleThe EMBO journal2021

PrimPol-mediated repriming facilitates replication traverse of DNA interstrand crosslinks.

Daniel González-Acosta, Elena Blanco-Romero, Patricia Ubieto-Capella, Karun Mutreja, Samuel Míguez, Susana Llanos, Fernando García, Javier Muñoz, Luis Blanco, Massimo Lopes and 1 more

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 69 citations in OpenAlex.

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  13. Accurate DNA Synthesis Across 8-Oxoadenine by Human PrimPol.International journal of molecular sciences · 2025
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  18. RAD52 prevents accumulation ofbioRxiv : the preprint server for biology · 2024
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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

11 authors at 3 institutions in 2 countries.

Daniel González-AcostaDNA Replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0003-3686-2297
Elena Blanco-RomeroDNA Replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0002-1340-2848
Patricia Ubieto-CapellaDNA Replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0002-1186-4643
Karun MutrejaInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Samuel MíguezDNA Replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0002-9279-6442
Susana LlanosDNA Replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0002-8555-9326
Fernando GarcíaProteomics Unit-ProteoRed-ISCIII, Biotechnology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0003-3888-4326
Javier MuñozProteomics Unit-ProteoRed-ISCIII, Biotechnology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0003-3288-3496
Luis BlancoCentro de Biología Molecular Severo Ochoa, CSIC-UAM, Madrid, Spain.ORCID 0000-0001-5558-4435
Massimo LopesInstitute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.ORCID 0000-0003-3847-8133
Juan MéndezDNA Replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.ORCID 0000-0002-3235-2559
Spanish National Cancer Research Centre · ESUniversity of Zurich · CHCentro de Biología Molecular Severo Ochoa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA interstrand crosslinks (ICLs) induced by endogenous aldehydes or chemotherapeutic agents interfere with essential processes such as replication and transcription. ICL recognition and repair by the Fanconi Anemia pathway require the formation of an X-shaped DNA structure that may arise from convergence of two replication forks at the crosslink or traversing of the lesion by a single replication fork. Here, we report that ICL traverse strictly requires DNA repriming events downstream of the lesion, which are carried out by PrimPol, the second primase-polymerase identified in mammalian cells after Polα/Primase. The recruitment of PrimPol to the vicinity of ICLs depends on its interaction with RPA, but not on FANCM translocase or the BLM/TOP3A/RMI1-2 (BTR) complex that also participate in ICL traverse. Genetic ablation of PRIMPOL makes cells more dependent on the fork convergence mechanism to initiate ICL repair, and PRIMPOL KO cells and mice display hypersensitivity to ICL-inducing drugs. These results open the possibility of targeting PrimPol activity to enhance the efficacy of chemotherapy based on DNA crosslinking agents.

Indexed as

AnimalsDNADNA-Directed DNA PolymeraseDNA HelicasesDNA PrimaseDNA RepairDNA ReplicationFemaleHumansMaleMammalsMiceMultifunctional EnzymesDNADNA-Directed DNA PolymeraseDNA HelicasesDNA PrimaseMultifunctional EnzymesPrimPol protein, humanICL repairICL traverseinterstrand crosslinkPrimPolRPA

Identifiers

PMID34128550
PMCPMC8280817
OpenAlexW3170693367

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.