Evidence map›Paper›PMID 40882638›Full record

ArticleStem cell reports2025

Inhibition of N-myristoyltransferase in pluripotent stem cells promotes the naive state in mice and elicits trophectoderm and primitive endoderm markers in humans.

Junko Yoshida, Hitomi Watanabe, Kaori Yamauchi, Takumi Nishikubo, Ayako Isotani, Satoshi Ohtsuka, Hitoshi Niwa, Yuki Kawamoto, Hidenori Akutsu, Akihiro Umezawa and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Junko YoshidaDepartment of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; Department of Genome Biology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Hitomi WatanabeLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Kaori YamauchiLaboratory of Embryonic Stem Cell Research, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Takumi NishikuboDepartment of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Ayako IsotaniGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan; Division of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5 Takayama-cho, Ikoma, Nara 630-0192, Japan.
Satoshi OhtsukaPluripotent Stem Cell Studies, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan; Laboratory for Experimental Animals, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.
Hitoshi NiwaPluripotent Stem Cell Studies, RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan; Department of Pluripotent Stem Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan.
Yuki KawamotoDepartment of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
Hidenori AkutsuCenter for Regenerative Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535, Japan.
Akihiro UmezawaCenter for Regenerative Medicine, National Center for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535, Japan.
Hirofumi SuemoriLaboratory of Embryonic Stem Cell Research, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Yasuhiro TakashimaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Hideo MatsudaDepartment of Bioinformatic Engineering, Graduate School of Information Science and Technology, Osaka University, 1-5 Yamadaoka, Suita, Osaka 565-0871, Japan.
Gen KondohLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Junji TakedaDepartment of Genome Biology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Laboratory of Immunoglycobiology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan. Electronic address: jjjtakeda@biken.osaka-u.ac.jp.
Kyoji HorieDepartment of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; Department of Genome Biology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Electronic address: k-horie@naramed-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Naive and primed states represent distinct phases of pluripotency during early embryonic development, both of which can be captured and interconverted in vitro. To understand pluripotency regulation, we performed a recessive genetic screen using homozygous mutant mouse embryonic stem cells (mESCs) and identified N-myristoyltransferase (NMT) as a novel regulator. Disruption of Nmt1 in mESCs conferred resistance to differentiation, and NMT suppression in mouse epiblast stem cells (mEpiSCs) promoted the conversion from the primed to the naive state. This effect was independent of proto-oncogene tyrosine-protein kinase Src (SRC), which is a major substrate of NMT and is known to promote mESC differentiation. In contrast, NMT suppression in naive-state human induced pluripotent stem cells (hiPSCs) partially induced naive markers but, more notably, expanded subpopulations expressing trophectoderm and primitive endoderm markers, most of which co-expressed the pluripotency marker POU5F1. These results identify NMT as a novel regulator of pluripotency, with distinct roles in mice and humans.

Indexed as

AcyltransferasesEndodermPluripotent Stem CellsAnimalsBiomarkersCell DifferentiationGerm LayersHumansInduced Pluripotent Stem CellsMiceMouse Embryonic Stem CellsProto-Oncogene MasAcyltransferasesBiomarkersglycylpeptide N-tetradecanoyltransferaseMAS1 protein, humanProto-Oncogene Masembryonic stem cellsepiblast stem cellsEpiSCsESCsinduced pluripotent stem cellsiPSCsnaive stateNMTN-myristoyltransferaseprimed stateSRC

Identifiers

PMID40882638
PMCPMC12447342

What OpenQuestion 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 OpenQuestion graph.