ArticleCell2013
Exit from pluripotency is gated by intracellular redistribution of the bHLH transcription factor Tfe3.
Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.
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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
208 citing papers in PubMed.
- Trial
- Suidae iPSC-derived macrophages as models for investigating susceptibility and resilience to African swine fever virus.Stem cell reports · 2026Article
- Article
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- Article
- The Cyclin C-CDK8/19 Mediator kinase module controls PRCC-TFE3 driven senescence in renal epithelium and tumorigenesis in TFE3-RCC.Neoplasia (New York, N.Y.) · 2026Article
- Review
- Metabolic oxidoreductases: central regulators of the epigenetic landscapes in stemness.Experimental & molecular medicine · 2026Review
- Exit from naive pluripotency proceeds with variable latency but without asymmetric division to generate population heterogeneity.Stem cell reports · 2026Article
- TDG orchestrates ATF4-dependent gene transcription during retinoic acid-induced cell fate acquisition.Nucleic acids research · 2026Article
- Cell-free DNA epigenomic profiling enables noninvasive detection and monitoring of translocation renal cell carcinoma.The Journal of clinical investigation · 2026Article
- Hyperactivation of mTORC1 blocks stem cell fate transitions through TFE3-NuRD association.EMBO reports · 2026Article
- Substrate-selective mTORC1 regulation and gene dosage-dependent tissue divergence in Birt-Hogg-Dubé syndrome.Frontiers in oncology · 2026Review
- Keeping up with the neighbours: local synchronisation of cell fate decisions during development.EMBO reports · 2026Review
- SFPQ-TFE3 reciprocally regulates mTORC1 and induces lineage plasticity in a mouse model of renal tumorigenesis.Nature communications · 2025Article
- The exit from naive pluripotency: a platform for the study of enhancer mechanistics.Biochemical Society transactions · 2025Review
- Repression of AGO1 by AGO2 via let-7 microRNAs facilitates embryonic stem cell differentiation.RNA (New York, N.Y.) · 2025Article
- Med12 cooperates with multiple differentiation signals to facilitate efficient lineage transitions in embryonic stem cells.Journal of cell science · 2025Article
- Propagating pluripotency - The conundrum of self-renewal.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Parallel genome-scale CRISPR-Cas9 screens uncouple human pluripotent stem cell identity versus fitness.Nature communications · 2024Article
148 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
Factors that sustain self-renewal of mouse embryonic stem cells (ESCs) are well described. In contrast, the machinery regulating exit from pluripotency is ill defined. In a large-scale small interfering RNA (siRNA) screen, we found that knockdown of the tumor suppressors Folliculin (Flcn) and Tsc2 prevent ESC commitment. Tsc2 lies upstream of mammalian target of rapamycin (mTOR), whereas Flcn acts downstream and in parallel. Flcn with its interaction partners Fnip1 and Fnip2 drives differentiation by restricting nuclear localization and activity of the bHLH transcription factor Tfe3. Conversely, enforced nuclear Tfe3 enables ESCs to withstand differentiation conditions. Genome-wide location and functional analyses showed that Tfe3 directly integrates into the pluripotency circuitry through transcriptional regulation of Esrrb. These findings identify a cell-intrinsic rheostat for destabilizing ground-state pluripotency to allow lineage commitment. Congruently, stage-specific subcellular relocalization of Tfe3 suggests that Flcn-Fnip1/2 contributes to developmental progression of the pluripotent epiblast in vivo.
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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.