Evidence map›Paper›PMID 40250406›Full record

ArticleCell chemical biology2025

Genetically encoded tool for manipulation of ΔΨm identifies its role as the driver of ISR induced by ATP synthase dysfunction.

Mangyu Choe, Alex E Ekvik, Gretchen Stalnaker, Hijai R Shin, Denis V Titov

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Mangyu ChoeDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA 94720, USA; Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Alex E EkvikDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA 94720, USA.
Gretchen StalnakerChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Hijai R ShinChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Denis V TitovDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, CA 94720, USA; Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Center for Computational Biology, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: titov@berkeley.edu.

Funding

UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2022 to 2026
$7.4M
Genetically encoded tools for manipulation of metabolism in vivoDP2GM132933 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI TITOV, DENIS VASILIEVICH · 2018 to 2018
$2.4M
Toward a quantitative understanding of metabolic homeostasisR35GM152114 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI Denis Vasilievich Titov · 2024 to 2026
$1.4M
NIDDK NIH HHS P30 DK127984NIGMS NIH HHS DP2 GM132933NIGMS NIH HHS R35 GM152114
6 · The paper itself

Abstract

Mitochondrial membrane potential (ΔΨm) is one of the key parameters controlling cellular bioenergetics. Investigation of the role of ΔΨm in live cells is complicated by a lack of tools for its direct manipulation without off-target effects. Here, we adopted the uncoupling protein UCP1 from brown adipocytes as a genetically encoded tool for direct manipulation of ΔΨm. We validated the ability of exogenously expressed UCP1 to induce uncoupled respiration and lower ΔΨm in mammalian cells. UCP1 expression lowered ΔΨm to the same extent as chemical uncouplers but did not inhibit cell proliferation, suggesting that it manipulates ΔΨm without the off-target effects of chemical uncouplers. Using UCP1, we revealed that elevated ΔΨm is the driver of the integrated stress response induced by ATP synthase inhibition in mammalian cells.

Indexed as

Membrane Potential, MitochondrialMitochondrial Proton-Translocating ATPasesUncoupling Protein 1AnimalsHEK293 CellsHumansMiceMitochondrial Proton-Translocating ATPasesUncoupling Protein 1ATP synthase inhibitionGEMMsgenetically encoded tools for manipulation of metabolismintegrated stress response,ISRmitochondrial membrane potentialUCP1ΔΨm

Identifiers

PMID40250406
PMCPMC12011318

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Registered trials

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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.