Evidence map›Paper›PMID 30690394›Full record

ArticleiScience2019

Mathematical Modeling Highlights the Complex Role of AKT in TRAIL-Induced Apoptosis of Colorectal Carcinoma Cells.

Matthew W Anderson, Joanna J Moss, Robert Szalai, Jon D Lane

Abstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Frontiers in systems biology · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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

4 authors.

Matthew W AndersonCentre for Biomedical Modelling and Analysis, Living Systems Institute, University of Exeter, Stocker Road, Exeter EX4 4QD, UK. Electronic address: m.w.anderson@exeter.ac.uk.
Joanna J MossCell Biology Laboratories, School of Biochemistry, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK.
Robert SzalaiDepartment of Engineering Mathematics, University of Bristol, Merchant Venturers Building, Woodland Road, Bristol BS8 1UB, UK.
Jon D LaneCell Biology Laboratories, School of Biochemistry, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK.

Funding

Wellcome Trust
6 · The paper itself

Abstract

Protein kinase B/AKT is a highly connected protein involved in a range of signaling pathways. Although it is known to regulate several proteins in the apoptotic pathway, its system-level effects remain poorly understood. We investigated the dynamic interactions between AKT and key apoptotic proteins and constructed a deterministic ordinary differential equation protein interaction model of extrinsic apoptosis. Incorporating AKT and its indirect inhibitor, phosphatase and tensin homolog (PTEN), this was used to generate predictions of system dynamics. Using eigen analysis, we identified AKT and cytochrome c as the protein species most sensitive to perturbations. Cell death assays in Type II HCT116 colorectal carcinoma cells revealed a tendency toward Type I cell death behavior in the XIAP

Indexed as

CancerCell BiologyIn Silico Biology

Identifiers

PMID30690394
PMCPMC6354781

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.