Evidence map›Paper›PMID 29107989›Full record

ArticlePLoS computational biology2017

Insight into glucocorticoid receptor signalling through interactome model analysis.

Emyr Bakker, Kun Tian, Luciano Mutti, Constantinos Demonacos, Jean-Marc Schwartz, Marija Krstic-Demonacos

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Relapse-associated AURKB blunts the glucocorticoid sensitivity of B cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  5. 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

6 authors at 2 institutions in 1 country.

Emyr BakkerBiomedical Research Centre, School of Environment and Life Sciences, University of Salford, Salford, United Kingdom.
Kun TianBiomedical Research Centre, School of Environment and Life Sciences, University of Salford, Salford, United Kingdom.
Luciano MuttiBiomedical Research Centre, School of Environment and Life Sciences, University of Salford, Salford, United Kingdom.
Constantinos DemonacosFaculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID http://orcid.org/0000-0002-4515-755X
Jean-Marc SchwartzFaculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Marija Krstic-DemonacosBiomedical Research Centre, School of Environment and Life Sciences, University of Salford, Salford, United Kingdom.ORCID http://orcid.org/0000-0002-3914-4488
University of Salford · GBUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid hormones (GCs) are used to treat a variety of diseases because of their potent anti-inflammatory effect and their ability to induce apoptosis in lymphoid malignancies through the glucocorticoid receptor (GR). Despite ongoing research, high glucocorticoid efficacy and widespread usage in medicine, resistance, disease relapse and toxicity remain factors that need addressing. Understanding the mechanisms of glucocorticoid signalling and how resistance may arise is highly important towards improving therapy. To gain insight into this we undertook a systems biology approach, aiming to generate a Boolean model of the glucocorticoid receptor protein interaction network that encapsulates functional relationships between the GR, its target genes or genes that target GR, and the interactions between the genes that interact with the GR. This model named GEB052 consists of 52 nodes representing genes or proteins, the model input (GC) and model outputs (cell death and inflammation), connected by 241 logical interactions of activation or inhibition. 323 changes in the relationships between model constituents following in silico knockouts were uncovered, and steady-state analysis followed by cell-based microarray genome-wide model validation led to an average of 57% correct predictions, which was taken further by assessment of model predictions against patient microarray data. Lastly, semi-quantitative model analysis via microarray data superimposed onto the model with a score flow algorithm has also been performed, which demonstrated significantly higher correct prediction ratios (average of 80%), and the model has been assessed as a predictive clinical tool using published patient microarray data. In summary we present an in silico simulation of the glucocorticoid receptor interaction network, linked to downstream biological processes that can be analysed to uncover relationships between GR and its interactants. Ultimately the model provides a platform for future development both by directing laboratory research and allowing for incorporation of further components, encapsulating more interactions/genes involved in glucocorticoid receptor signalling.

Indexed as

Computer SimulationModels, BiologicalAdolescentApoptosisChildChild, PreschoolFemaleGene Expression RegulationGene Regulatory NetworksGlucocorticoidsHumansMaleNeoplasmsProtein Interaction MapsReceptors, GlucocorticoidSignal TransductionGlucocorticoidsReceptors, Glucocorticoid

Identifiers

PMID29107989
PMCPMC5690696
OpenAlexW2767942532

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.