Evidence map›Paper›PMID 26225250›Full record

ArticleCPT: pharmacometrics & systems pharmacology2015

Dynamic Modeling of the Interaction Between Autophagy and Apoptosis in Mammalian Cells.

I Tavassoly, J Parmar, A N Shajahan-Haq, R Clarke, W T Baumann, J J Tyson

Open access · goldAbstract read
In one paragraph

Article in CPT: pharmacometrics & systems pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Dual regulation of autophagy: paradoxical effects on tumor angiogenesis.Frontiers in cell and developmental biology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Basal State Calibration of a Chemical Reaction Network Model for Autophagy.International journal of molecular sciences · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Mathematical Models of Death Signaling Networks.Entropy (Basel, Switzerland) · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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 3 institutions in 1 country.

I TavassolyGraduate Program in Genetics, Bioinformatics and Computational Biology, Virginia Polytechnic Institute and State University Blacksburg, Virginia, USA.
J ParmarDepartment of Biological Sciences, Virginia Polytechnic Institute and State University Blacksburg, Virginia, USA.
A N Shajahan-HaqLombardi Comprehensive Cancer Center, Georgetown University Medical Center Washington, DC, USA.
R ClarkeLombardi Comprehensive Cancer Center, Georgetown University Medical Center Washington, DC, USA.
W T BaumannBradley Department of Electrical and Computer Engineering, Virginia Polytechnic Institute and State University Blacksburg, Virginia, USA.
J J TysonDepartment of Biological Sciences, Virginia Polytechnic Institute and State University Blacksburg, Virginia, USA.
Virginia Tech · USGeorgetown University · USGeorgetown University Medical Center · US

Funding

Novel Targets in Endocrine ResponsivenessU54CA149147 · NCI · GEORGETOWN UNIVERSITY · PI MADHAVAN, SUBHA · 2010 to 2014
$6.9M
NCI NIH HHS U54 CA149147
6 · The paper itself

Abstract

Autophagy is a conserved biological stress response in mammalian cells that is responsible for clearing damaged proteins and organelles from the cytoplasm and recycling their contents via the lysosomal pathway. In cases of mild stress, autophagy acts as a survival mechanism, while in cases of severe stress cells may switch to programmed cell death. Understanding the decision process that moves a cell from autophagy to apoptosis is important since abnormal regulation of autophagy occurs in many diseases, including cancer. To integrate existing knowledge about this decision process into a rigorous, analytical framework, we built a mathematical model of cell fate decisions mediated by autophagy. Our dynamical model is consistent with existing quantitative measurements of autophagy and apoptosis in rat kidney proximal tubular cells responding to cisplatin-induced stress.

Identifiers

PMID26225250
PMCPMC4429580
OpenAlexW1935781822

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.