Evidence map›Paper›PMID 16672381›Full record

ArticleMolecular biology of the cell2006

The stress-activated mitogen-activated protein kinase signaling cascade promotes exit from mitosis.

Vladimír Reiser, Katharine E D'Aquino, Ly-Sha Ee, Angelika Amon

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.bioRxiv : the preprint server for biology · 2025
    Article
  3. The signalling lipid PI3,5POpen biology · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Hog1 activation delays mitotic exit via phosphorylation of Net1.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  8. The Multiple Roles of the Cdc14 Phosphatase in Cell Cycle Control.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Stressing mitosis to death.Frontiers in oncology · 2014
    Review
  15. Article
  16. Review
  17. Recovery from stress - a cell cycle perspective.Journal of computational interdisciplinary sciences · 2012
    Article
  18. Article
  19. Article
  20. Cellular functions of cardiolipin in yeast.Biochimica et biophysica acta · 2009
    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

4 authors at 1 institution in 1 country.

Vladimír ReiserCenter for Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Katharine E D'Aquino
Ly-Sha Ee
Angelika Amon
Howard Hughes Medical Institute · US

Funding

Regulation of Mitosis by Proteolysis in YeastR01GM056800 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI AMON, ANGELIKA B · 2004 to 2015
$3.4M
REGULATION OF MITOSIS BY PROTEOLYSIS IN YEASTR29GM056800 · NIGMS · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI AMON, ANGELIKA B · 1997 to 2003
$738k
NIGMS NIH HHS GM-56800NIGMS NIH HHS R01 GM056800NIGMS NIH HHS R29 GM056800
6 · The paper itself

Abstract

In budding yeast, a signaling network known as the mitotic exit network (MEN) triggers exit from mitosis. We find that hypertonic stress allows MEN mutants to exit from mitosis in a manner dependent on the high osmolarity glycerol (HOG) mitogen-activated protein (MAP) kinase cascade. The HOG pathway drives exit from mitosis in MEN mutants by promoting the activation of the MEN effector, the protein phosphatase Cdc14. Activation of Cdc14 depends on the Cdc14 early anaphase release network, a group of proteins that functions in parallel to the MEN to promote Cdc14 function. Notably, exit from mitosis is promoted by the signaling branch defined by the Sho1 osmosensing system, but not by the Sln1 osmosensor of the HOG pathway. Our results suggest that the stress MAP kinase pathway mobilizes programs to promote completion of the cell cycle and entry into G1 under unfavorable conditions.

Indexed as

MAP Kinase Signaling SystemMitosisCell CycleEnzyme ActivationFungal ProteinsG1 PhaseGlycerolHypertonic SolutionsMembrane ProteinsMutationOsmotic PressurePhosphoprotein PhosphatasesSaccharomycetalesSchizosaccharomyces pombe ProteinsCDC14 protein, S pombeFungal ProteinsGlycerolHypertonic SolutionsMembrane ProteinsPhosphoprotein PhosphatasesSchizosaccharomyces pombe Proteins

Identifiers

PMID16672381
PMCPMC1483046
OpenAlexW2097497257

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.