Evidence map›Paper›PMID 28396830›Full record

ArticleFEBS open bio2017

The G2 checkpoint-a node-based molecular switch.

Mark C de Gooijer, Arnout van den Top, Irena Bockaj, Jos H Beijnen, Thomas Würdinger, Olaf van Tellingen

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 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
3.3field-weighted citation impact, top 8% 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, 54 citations in OpenAlex.

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  17. The Role of Nitric Oxide in Cancer: Master Regulator or NOt?International journal of molecular sciences · 2020
    Review
  18. [Expression of CDC25A in non-small cell lung cancer and its relationship with let-7 gene].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    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

6 authors at 3 institutions in 2 countries.

Mark C de GooijerDivision of Pharmacology/Mouse Cancer Clinic The Netherlands Cancer Institute Amsterdam The Netherlands.
Arnout van den TopDivision of Pharmacology/Mouse Cancer Clinic The Netherlands Cancer Institute Amsterdam The Netherlands.
Irena BockajDivision of Pharmacology/Mouse Cancer Clinic The Netherlands Cancer Institute Amsterdam The Netherlands.
Jos H BeijnenDepartment of Pharmacy and Pharmacology The Netherlands Cancer Institute/Slotervaart Hospital Amsterdam The Netherlands; Division of Drug Toxicology Faculty of Pharmacy Utrecht University The Netherlands; Division of Biomedical Analysis Faculty of Science Utrecht University The Netherlands.
Thomas WürdingerNeuro-oncology Research Group Departments of Neurosurgery and Pediatric Oncology/Hematology Cancer Center Amsterdam VU University Medical Center The Netherlands; Molecular Neurogenetics Unit Departments of Neurology and Radiology Massachusetts General Hospital Boston MA USA; Neuroscience Program Harvard Medical School Boston MA USA.
Olaf van TellingenDivision of Pharmacology/Mouse Cancer Clinic The Netherlands Cancer Institute Amsterdam The Netherlands.
Cancer Genomics Centre · NLThe Netherlands Cancer Institute · NLHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tight regulation of the eukaryotic cell cycle is paramount to ensure genomic integrity throughout life. Cell cycle checkpoints are present in each phase of the cell cycle and prevent cell cycle progression when genomic integrity is compromised. The G2 checkpoint is an intricate signaling network that regulates the progression of G2 to mitosis (M). We propose here a node-based model of G2 checkpoint regulation, in which the action of the central CDK1-cyclin B1 node is determined by the concerted but opposing activities of the Wee1 and cell division control protein 25C (CDC25C) nodes. Phosphorylation of both Wee1 and CDC25C at specific sites determines their subcellular localization, driving them either toward activity within the nucleus or to the cytoplasm and subsequent ubiquitin-mediated proteasomal degradation. In turn, this subcellular balance of the Wee1 and CDC25C nodes is directed by the action of the PLK1 and CHK1 nodes via what we have termed the 'nuclear and cytoplasmic decision states' of Wee1 and CDC25C. The proposed node-based model provides an intelligible structure of the complex interactions that govern the decision to delay or continue G2/M progression. The model may also aid in predicting the effects of agents that target these G2 checkpoint nodes.

Indexed as

CDC25Ccell cycleCHK1G2 checkpointPLK1Wee1

Identifiers

PMID28396830
PMCPMC5377395
OpenAlexW2587102740

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.