Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.

Bing Pan, Fanghua Li, Emil Mladenov, Martin Stuschke, Beate Timmermann, George Iliakis

Abstract read

In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Bing PanInstitute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Fanghua LiInstitute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Emil MladenovInstitute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Martin StuschkeDivision of Experimental Radiation Biology, Department of Radiation Therapy, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Beate TimmermannDepartment of Particle Therapy, University Hospital Essen, West German Proton Therapy Centre Essen (WPE), West German Cancer Center (WTZ), German Cancer Consortium (DKTK), Essen, Germany.

George IliakisInstitute of Medical Radiation Biology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA double-strand breaks (DSBs) are highly cytotoxic lesions repaired primarily by homologous recombination (HR) and non-homologous end joining (NHEJ), with alternative end joining (alt-EJ) and single-strand annealing (SSA) functioning as backup. Repair pathway choice is governed by DNA end resection, suppressing NHEJ and committing repair to homology-based processes. Using pharmacological inhibition and protein depletion approaches in irradiated human cells, we show that PLK1 alone controls resection in S-phase-irradiated cells, while PLK1 and PLK3 act redundantly in G

Indexed as

Cell biologyDSB repairsMolecular interactionMolecular network

Identifiers

PMID42436985

DOI10.1016/j.isci.2026.116450

PMCPMC13355021

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LicenceCC BY

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Registered trials

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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.