ArticleCell reports2016
Glutamine Metabolism Regulates the Pluripotency Transcription Factor OCT4.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 95 citations in OpenAlex.
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- Tumor metabolic plasticity in therapy resistance: from the Warburg effect to mitochondrial hijacking.Theranostics · 2026Review
- SMAD3 and HIF-1α orchestrate metabolic transition to aerobic glycolysis as a critical prerequisite for spontaneous reprogramming of spermatogonial stem cells.Stem cell research & therapy · 2025Article
- Multiomics reveal biomolecular shifts and ER stress in sleep-restricted women affecting NSC functions.iScience · 2025Article
- Mitonuclear Communication in Stem Cell Function.Cell proliferation · 2025Review
- Physiological Modeling of the Vascularized Human Lung Organoid.American journal of respiratory cell and molecular biology · 2025Article
- Roe deer uterine fluid metabolome reveals elevated glycolysis, fatty acid breakdown, and spermidine synthesis upon reactivation from diapause†.Biology of reproduction · 2025Article
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- Metabolic adaptation pilots the differentiation of human hematopoietic cells.Life science alliance · 2024Article
- Oct4 redox sensitivity potentiates reprogramming and differentiation.Genes & development · 2024Article
- PRODH safeguards human naive pluripotency by limiting mitochondrial oxidative phosphorylation and reactive oxygen species production.EMBO reports · 2024Article
- Metabolism-regulating non-coding RNAs in breast cancer: roles, mechanisms and clinical applications.Journal of biomedical science · 2024Review
- Article
- Metabolic and proteostatic differences in quiescent and active neural stem cells.Neural regeneration research · 2024Review
- POZ/BTB and AT hook containing zinc finger 1 (PATZ1) suppresses differentiation and regulates metabolism in human embryonic stem cells.International journal of biological sciences · 2024Article
- MetaboLINK is a novel algorithm for unveiling cell-specific metabolic pathways in longitudinal datasets.Frontiers in neuroscience · 2024Article
- Non-metabolic enzyme function of pyruvate kinase M2 in breast cancer.Frontiers in oncology · 2024Review
- Mature mRNA processing that deletes 3' end sequences directs translational activation and embryonic development.Science advances · 2023Article
- The Role of ATP-Binding Cassette Proteins in Stem Cell Pluripotency.Biomedicines · 2023Review
- Targeting the Cysteine Redox Proteome in Parkinson's Disease: The Role of Glutathione Precursors and Beyond.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
The molecular mechanisms underlying the regulation of pluripotency by cellular metabolism in human embryonic stem cells (hESCs) are not fully understood. We found that high levels of glutamine metabolism are essential to prevent degradation of OCT4, a key transcription factor regulating hESC pluripotency. Glutamine withdrawal depletes the endogenous antioxidant glutathione (GSH), which results in the oxidation of OCT4 cysteine residues required for its DNA binding and enhanced OCT4 degradation. The emergence of the OCT4(lo) cell population following glutamine withdrawal did not result in greater propensity for cell death. Instead, glutamine withdrawal during vascular differentiation of hESCs generated cells with greater angiogenic capacity, thus indicating that modulating glutamine metabolism enhances the differentiation and functional maturation of cells. These findings demonstrate that the pluripotency transcription factor OCT4 can serve as a metabolic-redox sensor in hESCs and that metabolic cues can act in concert with growth factor signaling to orchestrate stem cell differentiation.
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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.