Evidence map›Paper›PMID 18716057›Full record

ArticleMolecular biology of the cell2008

Phosphatase inhibitor-2 balances protein phosphatase 1 and aurora B kinase for chromosome segregation and cytokinesis in human retinal epithelial cells.

Weiping Wang, P Todd Stukenberg, David L Brautigan

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. Regulation of PP1 interaction with I-2, neurabin, and F-actin.Molecular and cellular neurosciences · 2023
    Article
  5. Protein phosphatase-1 inhibitor-2 promotes PP1Frontiers in synaptic neuroscience · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Protein phosphatases in the regulation of mitosis.The Journal of cell biology · 2019
    Review
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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

3 authors at 2 institutions in 2 countries.

Weiping WangCenter for Cell Signaling, Departments of Microbiology and Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
P Todd Stukenberg
David L Brautigan
Toxicologie, Pharmacologie et Signalisation Cellulaire · FRUniversity of Virginia · US

Funding

Dissection of the Inner Centromere Regulatory NetworkR01GM063045 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BEKIRANOV, STEFAN, STUKENBERG, P. TODD · 2001 to 2013
$4.0M
Phosphorylation & Function of Inhibitor-2R01GM056362 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BRAUTIGAN, DAVID L. · 1997 to 2011
$2.4M
NIGMS NIH HHS GM-56362NIGMS NIH HHS GM-63045NIGMS NIH HHS R01 GM056362NIGMS NIH HHS R01 GM063045
6 · The paper itself

Abstract

Mitosis in Saccharomyces cerevisiae depends on IPL1 kinase, which genetically interacts with GLC8. The metazoan homologue of GLC8 is inhibitor-2 (I-2), but its function is not understood. We found endogenous and ectopic I-2 localized to the spindle, midzone, and midbody of mitotic human epithelial ARPE-19 cells. Knockdown of I-2 by RNA interference produced multinucleated cells, with supernumerary centrosomes, multipolar spindles and lagging chromosomes during anaphase. These defects did not involve changes in levels of protein phosphatase-1 (PP1), and the multinuclear phenotype was rescued by overexpression of I-2. Appearance of multiple nuclei and supernumerary centrosomes required progression through the cell cycle and I-2 knockdown cells failed cytokinesis, as observed by time-lapse microscopy. Inhibition of Aurora B by hesperadin produced multinucleated cells and reduced H3S10 phosphorylation. I-2 knockdown enhanced this latter effect. Partial knockdown of PP1Calpha prevented multiple nuclei caused by either knockdown of I-2 or treatment with hesperadin. Expression of enhanced green fluorescent protein-I-2 or hemagglutinin-I-2 made cells resistant to hesperadin. We propose that I-2 acts to enhance Aurora B by inhibiting specific PP1 holoenzymes that dephosphorylate Aurora B substrates necessary for chromosome segregation and cytokinesis. Conserved together throughout eukaryotic evolution, I-2, PP1 and Aurora B function interdependently during mitosis.

Indexed as

Chromosome SegregationCytokinesisAurora Kinase BAurora KinasesCell LineCell NucleusCentrosomeEpithelial CellsHistonesHumansIndolesMitosisModels, BiologicalPaclitaxelPhosphorylationProtein Kinase InhibitorsAURKB protein, humanAurora Kinase BAurora KinaseshesperadinHistonesIndolesPaclitaxelProtein Kinase InhibitorsProtein Phosphatase 1protein phosphatase inhibitor-2Protein Phosphatase Inhibitory ProteinsProteinsProtein Serine-Threonine KinasesSerineSulfonamides

Identifiers

PMID18716057
PMCPMC2575180
OpenAlexW2138545629

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.