Evidence map›Paper›PMID 28634351›Full record

ArticleScientific reports2017

A Dynamical Model for Activating and Silencing the Mitotic Checkpoint.

Richard Henze, Peter Dittrich, Bashar Ibrahim

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Trends in mathematical modeling of host-pathogen interactions.Cellular and molecular life sciences : CMLS · 2020
    Review
  10. Dissecting the mechanisms of cell division.The Journal of biological chemistry · 2019
    Review
  11. Article
  12. Article
  13. 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

3 authors.

Richard HenzeDepartment of Mathematics and Computer Science, Friedrich Schiller University Jena, 07743, Jena, Germany.
Peter DittrichDepartment of Mathematics and Computer Science, Friedrich Schiller University Jena, 07743, Jena, Germany.
Bashar IbrahimDepartment of Mathematics and Computer Science, Friedrich Schiller University Jena, 07743, Jena, Germany. bashar.ibrahim@uni-jena.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The spindle assembly checkpoint (SAC) is an evolutionarily conserved mechanism, exclusively sensitive to the states of kinetochores attached to microtubules. During metaphase, the anaphase-promoting complex/cyclosome (APC/C) is inhibited by the SAC but it rapidly switches to its active form following proper attachment of the final spindle. It had been thought that APC/C activity is an all-or-nothing response, but recent findings have demonstrated that it switches steadily. In this study, we develop a detailed mathematical model that considers all 92 human kinetochores and all major proteins involved in SAC activation and silencing. We perform deterministic and spatially-stochastic simulations and find that certain spatial properties do not play significant roles. Furthermore, we show that our model is consistent with in-vitro mutation experiments of crucial proteins as well as the recently-suggested rheostat switch behavior, measured by Securin or CyclinB concentration. Considering an autocatalytic feedback loop leads to an all-or-nothing toggle switch in the underlying core components, while the output signal of the SAC still behaves like a rheostat switch. The results of this study support the hypothesis that the SAC signal varies with increasing number of attached kinetochores, even though it might still contain toggle switches in some of its components.

Indexed as

Cell Cycle CheckpointsModels, BiologicalAlgorithmsMitosisMutationSpindle Apparatus

Identifiers

PMID28634351
PMCPMC5478649

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Registered trials

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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.