Evidence map›Paper›PMID 39495207›Full record

ArticleeLife2024

Perturbations in eIF3 subunit stoichiometry alter expression of ribosomal proteins and key components of the MAPK signaling pathways.

Anna Herrmannová, Jan Jelínek, Klára Pospíšilová, Farkas Kerényi, Tomáš Vomastek, Kathleen Watt, Jan Brábek, Mahabub Pasha Mohammad, Susan Wagner, Ivan Topisirovic and 1 more

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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

11 authors.

Anna Herrmannová *Laboratory of Regulation of Gene Expression, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.ORCID https://orcid.org/0000-0003-3500-3212
Jan Jelínek *Laboratory of Bioinformatics, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Klára PospíšilováLaboratory of Regulation of Gene Expression, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Farkas KerényiLaboratory of Regulation of Gene Expression, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Tomáš VomastekLaboratory of Cell Signaling, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Kathleen WattScience for Life Laboratory, Department of Oncology-Pathology, Karolinska Institutet, Solna, Sweden.ORCID https://orcid.org/0000-0001-6642-9756
Jan BrábekLady Davis Institute, Laboratory of Cancer Cell Invasion, Faculty of Science, Charles University, Prague, Czech Republic.
Mahabub Pasha MohammadLaboratory of Regulation of Gene Expression, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Susan WagnerLaboratory of Regulation of Gene Expression, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.
Ivan TopisirovicLady Davis Institute, Gerald Bronfman Department of Oncology, Department of Biochemistry, Division of Experimental Medicine, McGill University, Montréal, Canada.ORCID https://orcid.org/0000-0002-5510-9762
Leoš Shivaya ValášekLaboratory of Regulation of Gene Expression, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic.ORCID https://orcid.org/0000-0001-8123-8667

Funding

Akademie Věd České Republiky Praemium AcademiaeEuropean Union LX22NPO5102Fonds de Recherche du Québec - Santé Senior Investigator awardGrantová Agentura České Republiky 19-08013SGrantová Agentura České Republiky 19-25821XMinisterstvo Školství, Mládeže a Tělovýchovy CZ.02.01.01/00/22_008/0004575The Ministry of Education, Youth and Sports LM2023055
6 · The paper itself

Abstract

Protein synthesis plays a major role in homeostasis and when dysregulated leads to various pathologies including cancer. To this end, imbalanced expression of eukaryotic translation initiation factors (eIFs) is not only a consequence but also a driver of neoplastic growth. eIF3 is the largest, multi-subunit translation initiation complex with a modular assembly, where aberrant expression of one subunit generates only partially functional subcomplexes. To comprehensively study the effects of eIF3 remodeling, we contrasted the impact of eIF3d, eIF3e or eIF3h depletion on the translatome of HeLa cells using Ribo-seq. Depletion of eIF3d or eIF3e, but not eIF3h reduced the levels of multiple components of the MAPK signaling pathways. Surprisingly, however, depletion of all three eIF3 subunits increased MAPK/ERK pathway activity. Depletion of eIF3e and partially eIF3d also increased translation of TOP mRNAs that encode mainly ribosomal proteins and other components of the translational machinery. Moreover, alterations in eIF3 subunit stoichiometry were often associated with changes in translation of mRNAs containing short uORFs, as in the case of the proto-oncogene MDM2 and the transcription factor ATF4. Collectively, perturbations in eIF3 subunit stoichiometry exert specific effect on the translatome comprising signaling and stress-related transcripts with complex 5' UTRs that are implicated in homeostatic adaptation to stress and cancer.

Indexed as

Eukaryotic Initiation Factor-3MAP Kinase Signaling SystemProto-Oncogene MasRibosomal ProteinsHeLa CellsHumansProtein BiosynthesisEukaryotic Initiation Factor-3MAS1 protein, humanProto-Oncogene MasRibosomal ProteinseIF3geneticsgenomicshumanMAPK pathwayribosomal proteinsribosometranslationtranslational control

Identifiers

PMID39495207
PMCPMC11534336

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.