Evidence map›Paper›PMID 17360425›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Mechanism for inactivation of the mitotic inhibitory kinase Wee1 at M phase.

Kengo Okamoto, Noriyuki Sagata

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
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  6. Article
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  11. Review
  12. Review
  13. PIN1 in Cell Cycle Control and Cancer.Frontiers in pharmacology · 2018
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Filamin a regulates neural progenitor proliferation and cortical size through Wee1-dependent Cdk1 phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

2 authors.

Kengo OkamotoDepartment of Biology, Graduate School of Sciences, Kyushu University, Hakozaki 6-10-1, Fukuoka 812-8581, Japan.
Noriyuki Sagata

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wee1, the inhibitory kinase of cyclin B/Cdc2, undergoes a phosphorylation-dependent catalytic inactivation at M phase of the mitotic cell cycle, but the precise mechanism for this inactivation is not known. Using Xenopus egg and extract systems, we show here that the kinase activity of Xenopus somatic Wee1 (XeWee1B) is regulated by its N-terminal, small, well conserved region, termed here the Wee-box. The Wee-box is essential for the normal kinase activity of XeWee1B during interphase, acting positively on the C-terminal catalytic domain, which alone cannot efficiently phosphorylate Cdc2. Significantly, a Thr-186-Pro (TP) motif within the Wee-box is phosphorylated by Cdc2 at M phase and specifically binds the cis/trans prolyl isomerase Pin1. This Pin1 binding is required for the inactivation of XeWee1B at M phase, presumably causing isomerization of the phospho-TP motif and thereby impairing the function of the Wee-box. These results provide important insights into the mechanism of Wee1 inactivation at M phase.

Indexed as

Cell DivisionAmino Acid MotifsAmino Acid SequenceAnimalsCatalytic DomainCell Cycle ProteinsGene Expression RegulationInsectaMitosisMolecular Sequence DataNIMA-Interacting Peptidylprolyl IsomeraseOocytesPeptidylprolyl IsomerasePhosphorylationProtein BindingProtein-Tyrosine KinasesCell Cycle ProteinsNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomeraseProtein-Tyrosine KinasesWee2 protein, XenopusXenopus Proteins

Identifiers

PMID17360425
PMCPMC1820656

What OpenQuestion holds

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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.