ArticleNature communications2019
Folliculin regulates mTORC1/2 and WNT pathways in early human pluripotency.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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
33 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- Hyperactivation of mTORC1 blocks stem cell fate transitions through TFE3-NuRD association.EMBO reports · 2026Article
- Antagonistic roles for MITF and TFE3 in melanoma plasticity.Cell reports · 2025Article
- Advances in Molecular Mechanisms of Kidney Disease: Integrating Renal Tumorigenesis of Hereditary Cancer Syndrome.International journal of molecular sciences · 2024Review
- Derivation of Naïve Human Embryonic Stem Cells Using a CHK1 Inhibitor.Stem cell reviews and reports · 2023Article
- Influence of metabolic stress and metformin on synaptic protein profile in SH-SY5Y-derived neurons.Physiological reports · 2023Article
- Unveiling Novel Avenues in mTOR-Targeted Therapeutics: Advancements in Glioblastoma Treatment.International journal of molecular sciences · 2023Review
- Poly(ADP-Ribose) Polymerase-1 Lacking Enzymatic Activity Is Not Compatible with Mouse Development.Cells · 2023Article
- A critical role for heme synthesis and succinate in the regulation of pluripotent states transitions.eLife · 2023Article
- Golgi Stress Response: New Insights into the Pathogenesis and Therapeutic Targets of Human Diseases.Molecules and cells · 2023Review
- Familial multiple discoid fibromas is linked to a locus on chromosome 5 including the FNIP1 gene.Journal of human genetics · 2023Article
- Stress-induced reversible cell-cycle arrest requires PRC2/PRC1-mediated control of mitophagy in Drosophila germline stem cells and human iPSCs.Stem cell reports · 2023Article
- Review
- Crosstalk of organelles in Parkinson's disease - MiT family transcription factors as central players in signaling pathways connecting mitochondria and lysosomes.Molecular neurodegeneration · 2022Review
- Succinate as a New Actor in Pluripotency and Early Development?Metabolites · 2022Review
- Lysosomes at the Crossroads of Cell Metabolism, Cell Cycle, and Stemness.International journal of molecular sciences · 2022Review
- Birt-Hogg-Dubé Syndrome: Diagnostic Journey of Three Cases from Skin to Gene.Annals of dermatology · 2022Article
- KLF17 promotes human naïve pluripotency but is not required for its establishment.Development (Cambridge, England) · 2021Article
- The mTOR Pathway in Pluripotent Stem Cells: Lessons for Understanding Cancer Cell Dormancy.Membranes · 2021Review
- Folliculin haploinsufficiency causes cellular dysfunction of pleural mesothelial cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
To reveal how cells exit human pluripotency, we designed a CRISPR-Cas9 screen exploiting the metabolic and epigenetic differences between naïve and primed pluripotent cells. We identify the tumor suppressor, Folliculin(FLCN) as a critical gene required for the exit from human pluripotency. Here we show that FLCN Knock-out (KO) hESCs maintain the naïve pluripotent state but cannot exit the state since the critical transcription factor TFE3 remains active in the nucleus. TFE3 targets up-regulated in FLCN KO exit assay are members of Wnt pathway and ESRRB. Treatment of FLCN KO hESC with a Wnt inhibitor, but not ESRRB/FLCN double mutant, rescues the cells, allowing the exit from the naïve state. Using co-immunoprecipitation and mass spectrometry analysis we identify unique FLCN binding partners. The interactions of FLCN with components of the mTOR pathway (mTORC1 and mTORC2) reveal a mechanism of FLCN function during exit from naïve pluripotency.
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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.