Evidence map›Paper›PMID 32040547›Full record

ArticleThe Journal of cell biology2020

CDK1 couples proliferation with protein synthesis.

Katharina Haneke, Johanna Schott, Doris Lindner, Anne Kruse Hollensen, Christian Kroun Damgaard, Cyril Mongis, Michael Knop, Wilhelm Palm, Alessia Ruggieri, Georg Stoecklin

Abstract read
In one paragraph

Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing 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

64 citing papers in PubMed.

  1. Article
  2. Article
  3. TSC2 is a stress granule suppressor.bioRxiv : the preprint server for biology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Advances in ribosome profiling technologies.Biochemical Society transactions · 2025
    Review
  11. Article
  12. CDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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.

Katharina HanekeDivision of Biochemistry, Mannheim Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Johanna SchottDivision of Biochemistry, Mannheim Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Doris LindnerDivision of Biochemistry, Mannheim Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Anne Kruse HollensenDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Christian Kroun DamgaardDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Cyril MongisCenter for Molecular Biology of Heidelberg University, DKFZ-ZMBH Alliance, Heidelberg, Germany.
Michael KnopCenter for Molecular Biology of Heidelberg University, DKFZ-ZMBH Alliance, Heidelberg, Germany.
Wilhelm PalmCell Signaling and Metabolism, German Cancer Research Center, DKFZ-ZMBH Alliance, Heidelberg, Germany.
Alessia RuggieriDepartment of Infectious Diseases, Molecular Virology, Center for Integrative Infectious Diseases Research, University of Heidelberg, Heidelberg, Germany.
Georg StoecklinDivision of Biochemistry, Mannheim Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell proliferation exerts a high demand on protein synthesis, yet the mechanisms coupling the two processes are not fully understood. A kinase and phosphatase screen for activators of translation, based on the formation of stress granules in human cells, revealed cell cycle-associated kinases as major candidates. CDK1 was identified as a positive regulator of global translation, and cell synchronization experiments showed that this is an extramitotic function of CDK1. Different pathways including eIF2α, 4EBP, and S6K1 signaling contribute to controlling global translation downstream of CDK1. Moreover, Ribo-Seq analysis uncovered that CDK1 exerts a particularly strong effect on the translation of 5'TOP mRNAs, which includes mRNAs encoding ribosomal proteins and several translation factors. This effect requires the 5'TOP mRNA-binding protein LARP1, concurrent to our finding that LARP1 phosphorylation is strongly dependent on CDK1. Thus, CDK1 provides a direct means to couple cell proliferation with biosynthesis of the translation machinery and the rate of protein synthesis.

Indexed as

Cell ProliferationAdaptor Proteins, Signal TransducingAnimalsAutoantigensCDC2 Protein KinaseCell Cycle ProteinsEukaryotic Initiation Factor-2Eukaryotic Initiation FactorsFemaleFibroblastsGene Expression Regulation, EnzymologicHEK293 CellsHeLa CellsHumansKineticsMice, Inbred C57BLAdaptor Proteins, Signal TransducingAutoantigensCDC2 Protein KinaseCDK1 protein, humanCdk1 protein, mouseCell Cycle ProteinsEIF4EBP1 protein, humanEIF4EBP2 protein, humanEukaryotic Initiation Factor-2Eukaryotic Initiation FactorsRibonucleoproteinsribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDaRNA, MessengerSS-B Antigen

Identifiers

PMID32040547
PMCPMC7054999

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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.