Evidence map›Paper›PMID 37931173›Full record

ArticleStem cells (Dayton, Ohio)2024

Selective Inhibition of mTORC1 Signaling Supports the Development and Maintenance of Pluripotency.

Jin Koo Kim, Luis G Villa-Diaz, Thomas L Saunders, Ruiz P Saul, Suraj Timilsina, Fei Liu, Yuji Mishina, Paul H Krebsbach

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells (Dayton, Ohio), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 24% of its field
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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Spatial dynamics of mTOR pathway activity during bovine embryo development.Frontiers in cell and developmental biology · 2026
    Article
  3. 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

8 authors at 4 institutions in 1 country.

Jin Koo KimDivision of Oral and Systemic Health Sciences, University of California, Los Angeles School of Dentistry, Los Angeles, CA, USA.ORCID 0000-0003-4268-1118
Luis G Villa-DiazDepartment of Biological Sciences, Oakland University, Rochester, MI, USA.
Thomas L SaundersTransgenic Animal Model Core, University of Michigan, Ann Arbor, MI, USA.
Ruiz P SaulDepartment of Biological Sciences, Oakland University, Rochester, MI, USA.
Suraj TimilsinaStanford Shared FACS Facility, Stanford University, CA, USA.
Fei LiuDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA.
Yuji MishinaDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI, USA.
Paul H KrebsbachDivision of Oral and Systemic Health Sciences, University of California, Los Angeles School of Dentistry, Los Angeles, CA, USA.ORCID 0000-0001-9062-4981
University of Michigan · USOakland University · USUniversity of California, Los Angeles · USStanford Medicine · US

Funding

Molecular pathogenesis of craniosynostosis caused by enhanced BMP signalingR01DE020843 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MISHINA, YUJI · 2010 to 2019
$4.9M
Osteoblast Lineage Progression from Embryonic Stem CellsR01DE016530 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAARTINEN, VESA M · 2005 to 2016
$3.9M
NIDCR NIH HHS R01 DE016530NIDCR NIH HHS R01 DE020843NIH HHS R01DE016530
6 · The paper itself

Abstract

Insight into the molecular mechanisms governing the development and maintenance of pluripotency is important for understanding early development and the use of stem cells in regenerative medicine. We demonstrate the selective inhibition of mTORC1 signaling is important for developing the inner cell mass (ICM) and the self-renewal of human embryonic stem cells. S6K suppressed the expression and function of pluripotency-related transcription factors (PTFs) OCT4, SOX2, and KLF4 through phosphorylation and ubiquitin proteasome-mediated protein degradation, indicating that S6K inhibition is required for pluripotency. PTFs inhibited mTOR signaling. The phosphorylation of S6 was decreased in PTF-positive cells of the ICM in embryos. Activation of mTORC1 signaling blocked ICM formation and the selective inhibition of S6K by rapamycin increased the ICM size in mouse blastocysts. Thus, selective inhibition of mTORC1 signaling supports the development and maintenance of pluripotency.

Indexed as

BlastocystSignal TransductionAnimalsHumansMechanistic Target of Rapamycin Complex 1MicePhosphorylationSirolimusMechanistic Target of Rapamycin Complex 1Sirolimus4E-BP1human pluripotent stem cellsinner cell masspluripotency-related transcription factorsS6S6K

Identifiers

PMID37931173
PMCPMC10787279
OpenAlexW4388406746

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.