Evidence map›Paper›PMID 23509437›Full record

ArticlePLoS computational biology2013

Characterizing the relationship between steady state and response using analytical expressions for the steady states of mass action models.

Paul Michael Loriaux, Glenn Tesler, Alexander Hoffmann

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Computational modelling of aggressive B-cell lymphoma.Biochemical Society transactions · 2025
    Review
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  6. Review
  7. Computational modeling of DLBCL predicts response to BH3-mimetics.NPJ systems biology and applications · 2023
    Article
  8. Article
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  10. Review
  11. Nongenetic origins of cell-to-cell variability in B lymphocyte proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
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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 1 country.

Paul Michael LoriauxSignaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, California, United States of America.
Glenn Tesler
Alexander Hoffmann
University of California, San Diego · USCenter for Systems Biology · US

Funding

Information tranfer in NF-kappaB and MAPK pathwaysR01GM072024 · NIGMS · YALE UNIVERSITY · PI LEVCHENKO, ANDRE · 2004 to 2019
$3.9M
NIGMS NIH HHS GM072024NIGMS NIH HHS P50 GM085763NIGMS NIH HHS R01 GM072024PHS HHS CCF-1115206PHS HHS DMS-0718810
6 · The paper itself

Abstract

The steady states of cells affect their response to perturbation. Indeed, diagnostic markers for predicting the response to therapeutic perturbation are often based on steady state measurements. In spite of this, no method exists to systematically characterize the relationship between steady state and response. Mathematical models are established tools for studying cellular responses, but characterizing their relationship to the steady state requires that it have a parametric, or analytical, expression. For some models, this expression can be derived by the King-Altman method. However, King-Altman requires that no substrate act as an enzyme, and is therefore not applicable to most models of signal transduction. For this reason we developed py-substitution, a simple but general method for deriving analytical expressions for the steady states of mass action models. Where the King-Altman method is applicable, we show that py-substitution yields an equivalent expression, and at comparable efficiency. We use py-substitution to study the relationship between steady state and sensitivity to the anti-cancer drug candidate, dulanermin (recombinant human TRAIL). First, we use py-substitution to derive an analytical expression for the steady state of a published model of TRAIL-induced apoptosis. Next, we show that the amount of TRAIL required for cell death is sensitive to the steady state concentrations of procaspase 8 and its negative regulator, Bar, but not the other procaspase molecules. This suggests that activation of caspase 8 is a critical point in the death decision process. Finally, we show that changes in the threshold at which TRAIL results in cell death is not always equivalent to changes in the time of death, as is commonly assumed. Our work demonstrates that an analytical expression is a powerful tool for identifying steady state determinants of the cellular response to perturbation. All code is available at http://signalingsystems.ucsd.edu/models-and-code/ or as supplementary material accompanying this paper.

Indexed as

Models, BiologicalAntineoplastic AgentsCaspase 8Cell DeathComputational BiologyHeLa CellsHumansKineticsSignal TransductionTNF-Related Apoptosis-Inducing LigandAntineoplastic AgentsCaspase 8TNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID23509437
PMCPMC3585464
OpenAlexW2045164356

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.