Evidence map›Paper›PMID 29242632›Full record

ArticleScientific reports2017

Quantitative assessment of cell fate decision between autophagy and apoptosis.

Bing Liu, Zoltán N Oltvai, Hülya Bayır, Gary A Silverman, Stephen C Pak, David H Perlmutter, Ivet Bahar

Open access · goldAbstract 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 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.5field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Review
  4. Review
  5. Article
  6. Basal State Calibration of a Chemical Reaction Network Model for Autophagy.International journal of molecular sciences · 2024
    Article
  7. Review
  8. Epigenetic regulation ofAutophagy · 2024
    Review
  9. Review
  10. Review
  11. Life science alliance · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. PEBP1 acts as a rheostat between prosurvival autophagy and ferroptotic death in asthmatic epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    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

7 authors at 2 institutions in 1 country.

Bing LiuDepartment of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA, 15213, USA. liubing@pitt.edu.
Zoltán N OltvaiDepartment of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Hülya BayırDepartment of Critical Care Medicine, University of Pittsburgh, Pittsburgh, 15213, PA, USA.
Gary A SilvermanDepartment of Pediatrics, Washington University School of Medicine, St Louis, Missouri, MO, 63110, USA.
Stephen C PakDepartment of Pediatrics, Washington University School of Medicine, St Louis, Missouri, MO, 63110, USA.
David H PerlmutterDepartment of Pediatrics, Washington University School of Medicine, St Louis, Missouri, MO, 63110, USA.
Ivet BaharDepartment of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA, 15213, USA. bahar@pitt.edu.ORCID 0000-0001-9959-4176
University of Pittsburgh · USWashington University in St. Louis · US

Funding

Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
Treating AT Deficiency with Drugs that Modulate the Proteostasis NetworkP01DK096990 · NIDDK · WASHINGTON UNIVERSITY · PI FOX, IRA J. · 2012 to 2023
$18.3M
TrainingP41GM103712 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FAEDER, JAMES · 2012 to 2021
$16.3M
Genetic Modifiers Affecting Cellular Injury in Alpha-1-Antitrypsin DeficiencyR01DK104946 · NIDDK · WASHINGTON UNIVERSITY · PI SILVERMAN, GARY ARTHUR · 2016 to 2019
$1.4M
NIAID NIH HHS U19 AI068021NIDDK NIH HHS P01 DK096990NIDDK NIH HHS R01 DK104946NIGMS NIH HHS P41 GM103712
6 · The paper itself

Abstract

Autophagy and apoptosis are cellular processes that regulate cell survival and death, the former by eliminating dysfunctional components in the cell, the latter by programmed cell death. Stress signals can induce either process, and it is unclear how cells 'assess' cellular damage and make a 'life' or 'death' decision upon activating autophagy or apoptosis. A computational model of coupled apoptosis and autophagy is built here to analyze the underlying signaling and regulatory network dynamics. The model explains the experimentally observed differential deployment of autophagy and apoptosis in response to various stress signals. Autophagic response dominates at low-to-moderate stress; whereas the response shifts from autophagy (graded activation) to apoptosis (switch-like activation) with increasing stress intensity. The model reveals that cytoplasmic Ca

Indexed as

AMP-Activated Protein KinasesApoptosisAutophagyCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseCell SurvivalComputer SimulationCytoplasmEndoplasmic Reticulum StressHumansPhosphorylationSignal TransductionStress, PhysiologicalAMP-Activated Protein KinasesCalciumCalcium-Calmodulin-Dependent Protein Kinase Kinase

Identifiers

PMID29242632
PMCPMC5730598
OpenAlexW2953327471

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.