Evidence map›Paper›PMID 40328729›Full record

ArticleNature communications2025

mTORC1 cooperates with tRNA wobble modification to sustain the protein synthesis machinery.

Julia Hermann, Toman Borteçen, Robert Kalis, Alexander Kowar, Catarina Pechincha, Vivien Vogt, Martin Schneider, Dominic Helm, Jeroen Krijgsveld, Fabricio Loayza-Puch and 2 more

Abstract read
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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. RNA modifications in cancer and their detection: a review.Japanese journal of clinical oncology · 2026
    Review
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

12 authors.

Julia HermannDivision of Cell Signaling and Metabolism, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, Heidelberg, Germany.ORCID http://orcid.org/0009-0001-8545-4698
Toman BorteçenFaculty of Biosciences, University of Heidelberg, Heidelberg, Germany.
Robert KalisResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), Vienna, Austria.ORCID http://orcid.org/0000-0001-7553-4806
Alexander KowarFaculty of Biosciences, University of Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-7868-3935
Catarina PechinchaDivision of Cell Signaling and Metabolism, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-4650-4250
Vivien VogtResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), Vienna, Austria.
Martin SchneiderProteomics Core Facility, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Dominic HelmProteomics Core Facility, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0001-9321-2069
Jeroen KrijgsveldDivision of Proteomics of Stem Cells and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Fabricio Loayza-PuchTranslational Control and Metabolism Group, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0002-2999-8594
Johannes ZuberResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), Vienna, Austria.ORCID http://orcid.org/0000-0001-8810-6835
Wilhelm PalmDivision of Cell Signaling and Metabolism, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, Heidelberg, Germany. w.palm@dkfz-heidelberg.de.ORCID http://orcid.org/0000-0003-0612-770X

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC StG No. 759579Wilhelm Sander-Stiftung (Wilhelm Sander Foundation) Projektnummer 2024.086.1
6 · The paper itself

Abstract

Synthesizing the cellular proteome is a demanding process that is regulated by numerous signaling pathways and RNA modifications. How precisely these mechanisms control the protein synthesis machinery to generate specific proteome subsets remains unclear. Here, through genome-wide CRISPR screens we identify genes that enable mammalian cells to adapt to inactivation of the kinase mechanistic target of rapamycin complex 1 (mTORC1), the central driver of protein synthesis. When mTORC1 is inactive, enzymes that modify tRNAs at wobble uridines (U

Indexed as

Mechanistic Target of Rapamycin Complex 1Protein BiosynthesisRNA, TransferAnimalsCell Line, TumorCodonCRISPR-Cas SystemsGene Knockout TechniquesHumansMiceRibosomesUridineCodonMechanistic Target of Rapamycin Complex 1RNA, TransferUridine

Identifiers

PMID40328729
PMCPMC12056009

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.