Evidence map›Paper›PMID 28607002›Full record

ArticleThe EMBO journal2017

ATM/Wip1 activities at chromatin control Plk1 re-activation to determine G2 checkpoint duration.

Himjyot Jaiswal, Jan Benada, Erik Müllers, Karen Akopyan, Kamila Burdova, Tobias Koolmeister, Thomas Helleday, René H Medema, Libor Macurek, Arne Lindqvist

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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  4. TheLife (Basel, Switzerland) · 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

10 authors at 5 institutions in 3 countries.

Himjyot JaiswalDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Jan BenadaLaboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Erik MüllersDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Karen AkopyanDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Kamila BurdovaLaboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Tobias KoolmeisterDepartment of Medical Biochemistry and Biophysics, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Thomas HelledayDepartment of Medical Biochemistry and Biophysics, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
René H MedemaDivision of Cell Biology, Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-6754-0381
Libor MacurekLaboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic libor.macurek@img.cas.cz arne.lindqvist@ki.se.ORCID 0000-0002-0987-1238
Arne LindqvistDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden libor.macurek@img.cas.cz arne.lindqvist@ki.se.ORCID 0000-0002-0141-1579
Karolinska Institutet · SECzech Academy of Sciences, Institute of Molecular Genetics · CZScience for Life Laboratory · SECharles University · CZThe Netherlands Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After DNA damage, the cell cycle is arrested to avoid propagation of mutations. Arrest in G2 phase is initiated by ATM-/ATR-dependent signaling that inhibits mitosis-promoting kinases such as Plk1. At the same time, Plk1 can counteract ATR-dependent signaling and is required for eventual resumption of the cell cycle. However, what determines when Plk1 activity can resume remains unclear. Here, we use FRET-based reporters to show that a global spread of ATM activity on chromatin and phosphorylation of ATM targets including KAP1 control Plk1 re-activation. These phosphorylations are rapidly counteracted by the chromatin-bound phosphatase Wip1, allowing cell cycle restart despite persistent ATM activity present at DNA lesions. Combining experimental data and mathematical modeling, we propose a model for how the minimal duration of cell cycle arrest is controlled. Our model shows how cell cycle restart can occur before completion of DNA repair and suggests a mechanism for checkpoint adaptation in human cells.

Indexed as

G2 Phase Cell Cycle CheckpointsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineChromatinFluorescence Resonance Energy TransferHumansModels, BiologicalModels, TheoreticalPhosphorylationPolo-Like Kinase 1Protein Interaction MappingProtein Phosphatase 2CProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesProto-Oncogene ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsChromatinPolo-Like Kinase 1PPM1D protein, humanProtein Phosphatase 2CProtein Serine-Threonine KinasesProto-Oncogene ProteinsRepressor ProteinsTRIM28 protein, humanTripartite Motif-Containing Protein 28ATMATRcheckpoint recoveryG2Plk1

Identifiers

PMID28607002
PMCPMC5510006
OpenAlexW2625169780

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.