Evidence map›Paper›PMID 29254517›Full record

ArticleeLife2017

The CDK-PLK1 axis targets the DNA damage checkpoint sensor protein RAD9 to promote cell proliferation and tolerance to genotoxic stress.

Takeshi Wakida, Masae Ikura, Kenji Kuriya, Shinji Ito, Yoshiharu Shiroiwa, Toshiyuki Habu, Takuo Kawamoto, Katsuzumi Okumura, Tsuyoshi Ikura, Kanji Furuya

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022
    Review
  7. Article
  8. Review
  9. PLK1 targets NOTCH1 during DNA damage and mitotic progression.The Journal of biological chemistry · 2019
    Article
  10. Molecular cancer therapeutics · 2019
    Article
  11. Review
  12. Article
  13. Review
  14. 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

10 authors at 3 institutions in 1 country.

Takeshi WakidaDepartment of Radiation Systems, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Masae IkuraLaboratory of Chromatin Regulatory Network, Department of Mutagenesis, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Kenji KuriyaLaboratory of Nutritional Chemistry, Department of Life Sciences, Graduate School of Bioresources, Mie University, Tsu, Japan.
Shinji ItoMedical Research Support Center, Graduate School of Medicine, Kyoto University, Sakyo-ku, Japan.
Yoshiharu ShiroiwaDepartment of Radiation Systems, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Toshiyuki HabuDepartment of Radiation Systems, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Takuo KawamotoRadioisotope Research Center, Kyoto University, Kyoto, Japan.
Katsuzumi OkumuraLaboratory of Molecular and Cellular Biology, Department of Life Sciences, Mie University, Tsu, Japan.
Tsuyoshi IkuraLaboratory of Chromatin Regulatory Network, Department of Mutagenesis, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Kanji FuruyaDepartment of Radiation Systems, Radiation Biology Center, Kyoto University, Kyoto, Japan.ORCID 0000-0002-5099-8302
Kyoto University · JPMie University · JPMukogawa Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genotoxic stress causes proliferating cells to activate the DNA damage checkpoint, to assist DNA damage recovery by slowing cell cycle progression. Thus, to drive proliferation, cells must tolerate DNA damage and suppress the checkpoint response. However, the mechanism underlying this negative regulation of checkpoint activation is still elusive. We show that human

Indexed as

Cell ProliferationDNA DamageStress, PhysiologicalCell Cycle ProteinsCell LineCyclin-Dependent Kinase 2HumansMutagensPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsCDK2 protein, humanCell Cycle ProteinsCyclin-Dependent Kinase 2MutagensPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene Proteinsrad9 proteinchromosomesculture cellgenesHEK293humanU2OS

Identifiers

PMID29254517
PMCPMC5736350
OpenAlexW2779952267

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.