Evidence map›Paper›PMID 18056802›Full record

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

Control of mitotic exit by PP2A regulation of Cdc25C and Cdk1.

Craig M Forester, Jessica Maddox, Justin V Louis, Jozef Goris, David M Virshup

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 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

  1. Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025
    Review
  2. B56δ long-disordered arms form a dynamic PP2A regulation interface coupled with global allostery and Jordan's syndrome mutations.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Role of protein phosphatase 2A in kidney disease (Review).Experimental and therapeutic medicine · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Targeting PP2A in cancer: Combination therapies.Biochimica et biophysica acta. Molecular cell research · 2019
    Review
  19. Article
  20. Therapeutic targeting of PP2A.The international journal of biochemistry & cell biology · 2018
    Review
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

5 authors.

Craig M ForesterDepartment of Oncological Sciences and Center for Children, Huntsman Cancer Institute, Salt Lake City, UT 84112, USA.
Jessica Maddox
Justin V Louis
Jozef Goris
David M Virshup

Funding

TCF/LEF function during intestinal maintenance and colon tumorigenesisP01CA073992 · NCI · UNIVERSITY OF UTAH · PI NEKLASON, DEBORAH WOOD · 1998 to 2014
$29.7M
NCI NIH HHS P01 CA073992NCI NIH HHS P01 CA73992
6 · The paper itself

Abstract

Inactivation of maturation-promoting factor [(MPF) Cdk1/Cyclin B] is a key event in the exit from mitosis. Although degradation of Cyclin B is important for MPF inactivation, recent studies indicate that Cdk1 phosphorylation and inactivation occur before Cyclin B degradation and, therefore, also may be important steps in the exit from mitosis. Cdk1 activity is controlled by the Cdc25C phosphatase, which is turned on at the G(2)/M transition to catalyze Cdk1 activation. PP2A:B56delta is a negative regulator of Cdc25C during interphase. We show here that PP2A:B56delta also regulates Cdc25C at mitosis. Failure of PP2A:B56delta to dephosphorylate Cdc25C at mitosis results in prolonged hyperphosphorylation and activation of Cdc25C, causing persistent dephosphorylation and, hence, activation of Cdk1. This constitutive activation of Cdc25C and Cdk1 leads to a delayed exit from mitosis. Consistent with Cdk1 as a major biological target of B56delta, stable knockdown and germ-line mouse KO of B56delta leads to compensatory transcriptional up-regulation of Wee1 kinase to oppose the Cdc25C activity and permit cell survival. These observations place PP2A:B56delta as a key upstream regulator of Cdk1 activity upon exit from mitosis.

Indexed as

MitosisAnimalscdc25 PhosphatasesCDC2 Protein KinaseCell LineEnzyme ActivationGene Expression Regulation, EnzymologicHumansMesothelinMiceProtein BindingProtein Phosphatase 2Up-Regulationcdc25 PhosphatasesCDC2 Protein KinaseMesothelinMsln protein, mouseProtein Phosphatase 2

Identifiers

PMID18056802
PMCPMC2148389

What OpenQuestion holds

Textmetadata
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.