Genetically encoded tool for manipulation of ΔΨm identifies the latter as the driver of integrative stress response induced by ATP Synthase dysfunction.

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Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

Updated by
Genetically encoded tool for manipulation of ΔΨm identifies its role as the driver of ISR induced by ATP synthase dysfunction.2025

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Mangyu ChoeDepartment of Nutritional Sciences and Toxicology, University of California; Berkeley, CA 94720, USA.ORCID 0000-0002-8889-7494

Denis V TitovDepartment of Nutritional Sciences and Toxicology, University of California; Berkeley, CA 94720, USA.ORCID 0000-0001-5677-0651

Berkeley College · USUniversity of California, Berkeley · US

Funding

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

NIGMS 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.

Identifiers

PMID38234735

DOI10.1101/2023.12.27.573435

PMCPMC10793441

OpenAlexW4390297974

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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.