Evidence map›Paper›PMID 25392451›Full record

ArticleOpen biology2014

Targeting the INCENP IN-box-Aurora B interaction to inhibit CPC activity in vivo.

Florence H Gohard, Daniel J St-Cyr, Mike Tyers, William C Earnshaw

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Effect of PGV-1 on ApoptosisTurkish journal of pharmaceutical sciences · 2025
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  6. Cancer management and research · 2020
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Minimal model for collective kinetochore-microtubule dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  14. Review
  15. 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 2 institutions in 2 countries.

Florence H GohardWellcome Trust Centre for Cell Biology, Institute of Cell Biology, University of Edinburgh, Michael Swann Building, Kings Buildings, Mayfield Road, Edinburgh EH9 3JR, UK.
Daniel J St-CyrInstitute for Research in Immunology and Cancer, Department of Medicine, Université de Montréal, Pavillon Marcelle-Coutu, 2950 chemin de Polytechnique, Montréal, Québec H3T 1J4, Canada.ORCID http://orcid.org/0000-0003-2432-6585
Mike TyersWellcome Trust Centre for Cell Biology, Institute of Cell Biology, University of Edinburgh, Michael Swann Building, Kings Buildings, Mayfield Road, Edinburgh EH9 3JR, UK Institute for Research in Immunology and Cancer, Department of Medicine, Université de Montréal, Pavillon Marcelle-Coutu, 2950 chemin de Polytechnique, Montréal, Québec H3T 1J4, Canada.ORCID http://orcid.org/0000-0002-9713-9994
William C EarnshawWellcome Trust Centre for Cell Biology, Institute of Cell Biology, University of Edinburgh, Michael Swann Building, Kings Buildings, Mayfield Road, Edinburgh EH9 3JR, UK bill.earnshaw@ed.ac.uk.
Institute for Research in Immunology and Cancer · CAWellcome Centre for Cell Biology · GB

Funding

CIHREuropean Research Council 233457Wellcome Trust 073915Wellcome Trust 077707Wellcome Trust 085178Wellcome Trust 089396Wellcome Trust 092076
6 · The paper itself

Abstract

The chromosome passenger complex (CPC) is an essential regulator of mitosis and cytokinesis. The CPC consists of Aurora B kinase, inner centromere protein (INCENP), and the targeting subunits survivin and borealin/Dasra B. INCENP is a scaffolding subunit for the CPC and activates Aurora B via its conserved IN-box domain. We show that overexpression of soluble IN-box in HeLa cells affects endogenous CPC localization and produces a significant increase in multinucleated and micronucleated cells consistent with CPC loss of function. The dominant-negative effect of soluble IN-box expression depends on residues corresponding to hINCENP W845 and/or F881, suggesting that these are essential for Aurora B binding in vivo. We then screened a targeted library of small (five to nine residues long) circular peptide (CP) IN-box fragments generated using split intein circular ligation of proteins and peptides (SICLOPPS) methodology. We identified a number of CPs that caused modest but reproducible increases in rates of multinucleated and micronucleated cells. Our results provide proof of concept that inhibition of the Aurora B-IN-box interaction is a viable strategy for interfering with CPC function in vivo.

Indexed as

Amino Acid SequenceAurora Kinase BCell Cycle ProteinsChromosomal Proteins, Non-HistoneHeLa CellsHumansInhibitor of Apoptosis ProteinsMolecular Sequence DataPeptidesProtein BindingProtein Structure, TertiaryProtein TransportSmall Molecule LibrariesSurvivinAURKB protein, humanAurora Kinase BBIRC5 protein, humanCDCA8 protein, humanCell Cycle ProteinsChromosomal Proteins, Non-HistoneINCENP protein, humanInhibitor of Apoptosis ProteinsPeptidesSmall Molecule LibrariesSurvivinAurora Bchromosomal passenger complexcyclic peptidecytokinesisINCENPmitosis

Identifiers

PMID25392451
PMCPMC4248066
OpenAlexW2125676007

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.