Evidence map›Paper›PMID 28178678›Full record

ReviewOncotarget2017

The awakening of the CDK10/Cyclin M protein kinase.

Vincent J Guen, Carly Gamble, Jacqueline A Lees, Pierre Colas

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Genetic effects on the skin methylome in healthy older twins.American journal of human genetics · 2024
    Article
  9. Article
  10. Illumination of understudied ciliary kinases.Frontiers in molecular biosciences · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Distinct Signaling Pathways DistinguishFrontiers in cell and developmental biology · 2021
    Article
  17. Article
  18. CDKs in Sarcoma: Mediators of Disease and Emerging Therapeutic Targets.International journal of molecular sciences · 2020
    Review
  19. Review
  20. Development of a CDK10/CycMFrontiers in chemistry · 2020
    Article
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

4 authors at 3 institutions in 2 countries.

Vincent J GuenDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, United States of America.
Carly GambleP2I2 Group, Protein Phosphorylation and Human Disease Laboratory, Station Biologique de Roscoff, Centre National de la Recherche Scientifique, Université Pierre et Marie Curie, Roscoff, France.
Jacqueline A LeesDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, United States of America.
Pierre ColasP2I2 Group, Protein Phosphorylation and Human Disease Laboratory, Station Biologique de Roscoff, Centre National de la Recherche Scientifique, Université Pierre et Marie Curie, Roscoff, France.
Massachusetts Institute of Technology · USCentre National de la Recherche Scientifique · FRStation Biologique de Roscoff · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinases (CDKs) play important roles in the control of fundamental cellular processes. Some of the most characterized CDKs are considered to be pertinent therapeutic targets for cancers and other diseases, and first clinical successes have recently been obtained with CDK inhibitors. Although discovered in the pre-genomic era, CDK10 attracted little attention until it was identified as a major determinant of resistance to endocrine therapy for breast cancer. In some studies, CDK10 has been shown to promote cell proliferation whereas other studies have revealed a tumor suppressor function. The recent discovery of Cyclin M as a CDK10 activating partner has allowed the unveiling of a protein kinase activity against the ETS2 oncoprotein, whose degradation is activated by CDK10/Cyclin M-mediated phosphorylation. CDK10/Cyclin M has also been shown to repress ciliogenesis and to maintain actin network architecture, through the phoshorylation of the PKN2 protein kinase and the control of RhoA stability. These findings shed light on the molecular mechanisms underlying STAR syndrome, a severe human developmental genetic disorder caused by mutations in the Cyclin M coding gene. They also pave the way to a better understanding of the role of CDK10/Cyclin M in cancer.

Indexed as

Cyclin-Dependent KinasesCyclinsHumansProtein Kinase CCDK10 protein, humanCyclin-Dependent KinasesCyclinsProtein Kinase CCDK10ciliogenesisCyclin METS2STAR syndrome

Identifiers

PMID28178678
PMCPMC5564841
OpenAlexW2584293815

What OpenQuestion holds

Textmetadata
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.