Evidence map›Paper›PMID 28345297›Full record

ArticleAging cell2017

Residual Cdk1/2 activity after DNA damage promotes senescence.

Erik Müllers, Helena Silva Cascales, Kamila Burdova, Libor Macurek, Arne Lindqvist

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-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

32 citing papers in PubMed, 51 citations in OpenAlex.

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  15. Polyploid giant cancer cells and cancer progression.Frontiers in cell and developmental biology · 2022
    Review
  16. Mechanisms and Regulation of Cellular Senescence.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. Article
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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

5 authors at 2 institutions in 2 countries.

Erik MüllersDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Helena Silva CascalesDepartment 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.
Libor MacurekLaboratory of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Arne LindqvistDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-0141-1579
Karolinska Institutet · SECzech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In response to DNA damage, a cell can be forced to permanently exit the cell cycle and become senescent. Senescence provides an early barrier against tumor development by preventing proliferation of cells with damaged DNA. By studying single cells, we show that Cdk activity persists after DNA damage until terminal cell cycle exit. This low level of Cdk activity not only allows cell cycle progression, but also promotes cell cycle exit at a decision point in G2 phase. We find that residual Cdk1/2 activity is required for efficient p21 production, allowing for nuclear sequestration of Cyclin B1, subsequent APC/C

Indexed as

Antigens, CDCadherinsCDC2 Protein KinaseCell LineCell Line, TumorCell SizeCell SurvivalCellular SenescenceCyclin B1Cyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21DNA DamageEpithelial CellsEtoposideG2 Phase Cell Cycle CheckpointsGene Expression Regulation4-(6-cyclohexylmethoxy-9H-purin-2-ylamino)-N,N-diethylbenzamideAntigens, CDBI 2536CadherinsCCNB1 protein, humanCDC2 Protein KinaseCDH1 protein, humanCDK1 protein, humanCDK2 protein, humanCyclin B1Cyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21EtoposidePteridinesPurinesQuinolinesRO 3306ThiazolesCdk1Cdk2cell cyclecheckpoint recoveryDNA damage responseG2 phasep21senescence

Identifiers

PMID28345297
PMCPMC5418196
OpenAlexW2597897076

What OpenQuestion holds

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LicenceCC BY
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.