ArticleCell stem cell2017
MYC Controls Human Pluripotent Stem Cell Fate Decisions through Regulation of Metabolic Flux.
Article in Cell stem cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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.
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.
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Who cites it
90 citing papers in PubMed, 152 citations in OpenAlex.
- CircACVR2A(2-4) regulates stem cell pluripotency by uncoupling CDK-activating kinase functions.Nucleic acids research · 2026Article
- TGFβ-dependent upregulation of OCIAD2 is essential for epithelial-to-mesenchymal transition during mesendoderm differentiation.Stem cell reports · 2026Article
- Metabolic Programming of β-Cell Fate, State, and Function through Time and Space.Physiology (Bethesda, Md.) · 2026Review
- JMJD3-mediated HADH demethylation orchestrates hepatocyte maturation through fatty acid β-oxidation-dependent histone acetylation.Experimental & molecular medicine · 2026Article
- Loss of E3 Ubiquitin Ligase RINES via CpG Methylation Relieves Suppression of STAT3 and MYC, Facilitating Multiple Tumorigeneses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- (+)-Miliusol suppresses the Warburg effect and induces regulated cell death in triple-negative breast cancer through targeting EIF3D and remodeling cancer metabolism.Acta pharmaceutica Sinica. B · 2026Article
- Reprogramming lipid metabolism in pediatric cancers.Oncogenesis · 2026Review
- TGFβ-activated PDHB promotes mitochondrial pyruvate metabolism and contributes to human endoderm differentiation via ATP-dependent BRG1.Nature communications · 2026Article
- From fitness to fate: Hippo-YAP-mediated cell competition influence on stem cells activity.Bioscience reports · 2026Review
- Genetic screening of long non-coding RNAs in human embryonic stem cells reveals novel regulators of pluripotency.Stem cell reports · 2026Article
- Mitochondrial development and remodeling occur at pancreatic progenitor stage during induction of stem cell-derived islet organoids.Frontiers in endocrinology · 2026Article
- How one nutrient controls cell size.eLife · 2025Article
- Decoding the lactylation-immune link in calcific aortic valve disease: a comprehensive bioinformatics approach.Human genomics · 2025Article
- Mitochondrial dysfunction by glyoxalase 1 deficiency disrupts definitive endoderm and alveolar development of human pluripotent stem cells.Experimental & molecular medicine · 2025Article
- Article
- Serine synthesis pathway regulates cardiac differentiation from human pluripotent stem cells.iScience · 2025Article
- Glycolytic activity instructs germ layer proportions through regulation of Nodal and Wnt signaling.Cell stem cell · 2025Article
- X-Linked Gene Dosage and SOX2 Act as Key Roadblocks for Human Germ Cell Specification in Klinefelter Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unveiling distinctions between mesenchymal stromal cells and stem cells by single-cell transcriptomic analysis.Heliyon · 2025Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
As human pluripotent stem cells (hPSCs) exit pluripotency, they are thought to switch from a glycolytic mode of energy generation to one more dependent on oxidative phosphorylation. Here we show that, although metabolic switching occurs during early mesoderm and endoderm differentiation, high glycolytic flux is maintained and, in fact, essential during early ectoderm specification. The elevated glycolysis observed in hPSCs requires elevated MYC/MYCN activity. Metabolic switching during endodermal and mesodermal differentiation coincides with a reduction in MYC/MYCN and can be reversed by ectopically restoring MYC activity. During early ectodermal differentiation, sustained MYCN activity maintains the transcription of "switch" genes that are rate-limiting for metabolic activity and lineage commitment. Our work, therefore, shows that metabolic switching is lineage-specific and not a required step for exit of pluripotency in hPSCs and identifies MYC and MYCN as developmental regulators that couple metabolism to pluripotency and cell fate determination.
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Registered trials
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.