Evidence map›Paper›PMID 38177915›Full record

ArticleEMBO reports2024

A beneficial adaptive role for CHOP in driving cell fate selection during ER stress.

Kaihua Liu, Chaoxian Zhao, Reed C Adajar, Diane DeZwaan-McCabe, D Thomas Rutkowski

Open access · diamondAbstract read
In one paragraph

Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
9.8field-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

24 citing papers in PubMed, 31 citations in OpenAlex.

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  18. ER-tethered stress sensor CREBH regulates mitochondrial unfolded protein response to maintain energy homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Kaihua LiuInterdisciplinary Graduate Program in Human Toxicology, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Chaoxian ZhaoShanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0002-7126-0841
Reed C AdajarDepartment of Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Diane DeZwaan-McCabeDepartment of Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
D Thomas RutkowskiInterdisciplinary Graduate Program in Human Toxicology, University of Iowa Carver College of Medicine, Iowa City, IA, USA. thomas-rutkowski@uiowa.edu.ORCID http://orcid.org/0000-0001-6586-4449
University of Iowa · USShanghai Jiao Tong University · CN

Funding

Vector Core-Core 2P30DK054759 · NIDDK · UNIVERSITY OF IOWA · PI Alejandro Antonio Pezzulo · 1998 to 2026
$30.5M
Regulation of Fatty Acid Oxidation during ER stress: mechanisms and consequencesR01GM115424 · NIGMS · UNIVERSITY OF IOWA · PI RUTKOWSKI, DAVID THOMAS · 2015 to 2023
$2.5M
NIDDK NIH HHS P30 DK054759NIGMS NIH HHS R01 GM115424
6 · The paper itself

Abstract

Cellular stresses elicit signaling cascades that are capable of either mitigating the inciting dysfunction or initiating cell death. During endoplasmic reticulum (ER) stress, the transcription factor CHOP is widely recognized to promote cell death. However, it is not clear whether CHOP also has a beneficial role during adaptation. Here, we combine a new, versatile, genetically modified Chop allele with single cell analysis and with stresses of physiological intensity, to rigorously examine the contribution of CHOP to cell fate. Paradoxically, we find that CHOP promotes death in some cells, but proliferation-and hence recovery-in others. Strikingly, this function of CHOP confers to cells a stress-specific competitive growth advantage. The dynamics of CHOP expression and UPR activation at the single cell level suggest that CHOP maximizes UPR activation, which in turn favors stress resolution, subsequent UPR deactivation, and proliferation. Taken together, these findings suggest that CHOP's function can be better described as a "stress test" that drives cells into either of two mutually exclusive fates-adaptation or death-during stresses of physiological intensity.

Indexed as

Endoplasmic Reticulum StressSignal TransductionCell DeathTranscription Factor CHOPUnfolded Protein ResponseTranscription Factor CHOPAdaptation; Cell Fate; ER Stress; Cell Proliferation; Unfolded Protein Response

Identifiers

PMID38177915
PMCPMC10897205
OpenAlexW4390498432

What OpenQuestion holds

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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.