Evidence map›Paper›PMID 24316673›Full record

ArticleNature cell biology2014

Autophagy variation within a cell population determines cell fate through selective degradation of Fap-1.

Jacob M Gump, Leah Staskiewicz, Michael J Morgan, Alison Bamberg, David W H Riches, Andrew Thorburn

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.

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87 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Jacob M GumpDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045, USA.
Leah StaskiewiczDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045, USA.
Michael J MorganDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045, USA.
Alison BambergDepartment of Pediatrics, National Jewish Health, Denver, Colorado 80206, USA.
David W H RichesDepartment of Pediatrics, National Jewish Health, Denver, Colorado 80206, USA.
Andrew ThorburnDepartment of Pharmacology, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045, USA.
University of Colorado Anschutz Medical Campus · USNational Jewish Health · USUniversity of Colorado Denver · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Role of autophagy in tumor cell deathR01CA150925 · NCI · UNIVERSITY OF COLORADO DENVER · PI DEGREGORI, JAMES V · 2010 to 2024
$5.5M
POSTGRADUATE TRAINING IN PEDIATRIC ONCOLOGYT32CA082086 · NCI · UNIVERSITY OF COLORADO DENVER · PI GORE, LIA · 2000 to 2015
$4.1M
Mechanisms of myofibroblast survival in fibrosisR01HL068628 · NHLBI · NATIONAL JEWISH HEALTH · PI RICHES, DAVID W. · 2002 to 2011
$3.4M
FADD Signaling in Cancer CellsR01CA111421 · NCI · UNIVERSITY OF COLORADO DENVER · PI THORBURN, ANDREW M · 2005 to 2014
$2.8M
DUSP1 as a therapeutic target in fibroproliferative acute lung injuryR01HL114754 · NHLBI · NATIONAL JEWISH HEALTH · PI RICHES, DAVID W. · 2013 to 2016
$1.6M
NCI NIH HHS 5T32CA82086-10NCI NIH HHS CA150925NCI NIH HHS P30 CA046934NCI NIH HHS P30 CA46934NCI NIH HHS R01 CA111421NCI NIH HHS R01 CA150925NCI NIH HHS T32 CA082086NHLBI NIH HHS HL68628NHLBI NIH HHS R01 HL068628NHLBI NIH HHS R01 HL114754
6 · The paper itself

Abstract

Autophagy regulates cell death both positively and negatively, but the molecular basis for this paradox remains inadequately characterized. We demonstrate here that transient cell-to-cell variations in autophagy can promote either cell death or survival depending on the stimulus and cell type. By separating cells with high and low basal autophagy using flow cytometry, we demonstrate that autophagy determines which cells live or die in response to death receptor activation. We have determined that selective autophagic degradation of the phosphatase Fap-1 promotes Fas apoptosis in Type I cells, which do not require mitochondrial permeabilization for efficient apoptosis. Conversely, autophagy inhibits apoptosis in Type II cells (which require mitochondrial involvement) or on treatment with TRAIL in either Type I or II cells. These data illustrate that differences in autophagy in a cell population determine cell fate in a stimulus- and cell-type-specific manner. This example of selective autophagy of an apoptosis regulator may represent a general mechanism for context-specific regulation of cell fate by autophagy.

Indexed as

AutophagyCell LineageProteolysisAdaptor Proteins, Signal TransducingApoptosisCell ProliferationCell SurvivalChloroquineCulture MediaFas Ligand Proteinfas ReceptorGreen Fluorescent ProteinsHeLa CellsHumansJurkat CellsModels, BiologicalAdaptor Proteins, Signal TransducingChloroquineCulture MediaFas Ligand ProteinFAS protein, humanfas ReceptorGreen Fluorescent ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 13PTPN13 protein, humanRecombinant Fusion ProteinsSequestosome-1 ProteinSQSTM1 protein, human

Identifiers

PMID24316673
PMCPMC3876036
OpenAlexW2081826742

What OpenQuestion holds

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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.