Evidence map›Paper›PMID 40203091›Full record

ArticleScience advances2025

EIF3D safeguards the homeostasis of key signaling pathways in human primed pluripotency.

Chikako Okubo, Michiko Nakamura, Masae Sato, Yuichi Shichino, Mari Mito, Yasuhiro Takashima, Shintaro Iwasaki, Kazutoshi Takahashi

Abstract read
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. 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

8 authors.

Chikako OkuboDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.ORCID 0000-0001-5562-410X
Michiko NakamuraDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.ORCID 0000-0002-6778-9320
Masae SatoDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.ORCID 0009-0005-8805-9676
Yuichi ShichinoRNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, Saitama, 351-0198, Japan.ORCID 0000-0002-0093-1185
Mari MitoRNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, Saitama, 351-0198, Japan.ORCID 0000-0003-2564-6273
Yasuhiro TakashimaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.ORCID 0000-0003-0126-7260
Shintaro IwasakiRNA Systems Biochemistry Laboratory, RIKEN Cluster for Pioneering Research, Saitama, 351-0198, Japan.ORCID 0000-0001-7724-3754
Kazutoshi TakahashiDepartment of Life Science Frontiers, Center for iPS Cell Research and Application, Kyoto University, Kyoto, 606-8507, Japan.ORCID 0000-0002-5329-8395

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although pluripotent stem cell (PSC) properties, such as differentiation and infinite proliferation, have been well documented within the frameworks of transcription factor networks, epigenomes, and signal transduction, they remain unclear and fragmented. Directing attention toward translational regulation as a bridge between these events can yield additional insights into previously unexplained mechanisms. Our functional CRISPR interference screen-based approach revealed that EIF3D, a translation initiation factor, is crucial for maintaining primed pluripotency. Loss of EIF3D disrupted the balance of pluripotency-associated signaling pathways, thereby compromising primed pluripotency. Moreover, EIF3D ensured robust proliferation by controlling the translation of various p53 regulators, which maintain low p53 activity in the undifferentiated state. In this way, EIF3D-mediated translation contributes to tuning the homeostasis of the primed pluripotency networks, ensuring the maintenance of an undifferentiated state with high proliferative potential. This study provides further insights into the translation network in maintaining pluripotency.

Indexed as

Eukaryotic Initiation Factor-3HomeostasisPluripotent Stem CellsSignal TransductionCell DifferentiationCell ProliferationHumansTumor Suppressor Protein p53Eukaryotic Initiation Factor-3Tumor Suppressor Protein p53

Identifiers

PMID40203091
PMCPMC11980838

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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.