Evidence map›Paper›PMID 41339359›Full record

ArticleNature communications2025

Vacuolar-type H

Geoffray Monteuuis, Ryan Awadhpersad, Daan van der Kolk, Sachin K Singh, Tuula A Nyman, Alina Malyutina, Nicola Zamboni, Kari Moisio, Juhana Juutila, Ville Hietakangas and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

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

1 citing paper in PubMed.

  1. [ATPase HZhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    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

13 authors.

Geoffray MonteuuisDepartment of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Ryan AwadhpersadDepartment of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0001-8810-1786
Daan van der KolkDepartment of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Sachin K SinghDepartment of Immunology, Institute of Clinical Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway.
Tuula A NymanDepartment of Immunology, Institute of Clinical Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway.ORCID http://orcid.org/0000-0001-8787-5886
Alina MalyutinaResearch Program in Systems Oncology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Nicola ZamboniInstitute of Molecular Systems Biology, Department of Biology, ETH Zurich, Zurich, Switzerland.ORCID http://orcid.org/0000-0003-1271-1021
Kari MoisioFaculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland.
Juhana JuutilaFaculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland.
Ville HietakangasFaculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland.ORCID http://orcid.org/0000-0002-9900-7549
Sara SenecaCenter for Medical Genetics/Research Center Reproduction and Genetics, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Christopher J CarrollGenetics Section, Cardiovascular and Genomics Research Institute, City St. George's, University of London, London, UK.ORCID http://orcid.org/0000-0002-2814-6955
Christopher B JacksonDepartment of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland. christopher.jackson@helsinki.fi.ORCID http://orcid.org/0000-0003-1035-6417

Funding

Academy of Finland (Suomen Akatemia) 336455Jane ja Aatos Erkon Säätiö (Jane and Aatos Erkko Foundation) 230004
6 · The paper itself

Abstract

Mitochondrial dysfunction underlies a wide range of human diseases, including primary mitochondrial disorders, neurodegeneration, cancer, and ageing. To preserve cellular homeostasis, organisms have evolved adaptive mechanisms that coordinate nuclear and mitochondrial gene expression. Here, we use genome-wide CRISPR knockout screening to identify cell fitness pathways that support survival under impaired mitochondrial protein synthesis. The strongest suppressor of aberrant mitochondrial translation defects - besides a compendium of known mitochondrial translation quality control factors - is the loss of the vacuolar-type H

Indexed as

MitochondriaMitochondrial DiseasesVacuolar Proton-Translocating ATPasesCell Line, TumorHomeostasisHumansHydrogen-Ion ConcentrationMembrane Potential, MitochondrialProtein BiosynthesisVacuolar Proton-Translocating ATPases

Identifiers

PMID41339359
PMCPMC12769673

What Socratic 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 Socratic graph.