ArticleNature communications2020
mTOR and S6K1 drive polycystic kidney by the control of Afadin-dependent oriented cell division.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- USP21-mediated deubiquitylation stimulates NuMA recruitment to the cell cortex to promote mitotic spindle orientation.Cell death and differentiation · 2026Article
- Folliculin Deletion in the Mouse Kidney Results in Cystogenesis of the Loops of Henle via Aberrant TFEB Activation.The American journal of pathology · 2025Article
- Impact of Mlkl or Ripk3 deletion on age-associated liver inflammation, metabolic health, and lifespan.GeroScience · 2025Article
- Targeting interleukin-1 signaling for renoprotection.Frontiers in immunology · 2025Review
- Review
- The Spectrum of Renal "TFEopathies": Flipping the mTOR Switch in Renal Tumorigenesis.Physiology (Bethesda, Md.) · 2024Review
- mTORC1 signaling and diabetic kidney disease.Diabetology international · 2024Review
- mTOR/miR-142-3p/PRAS40 signaling cascade is critical for tuberous sclerosis complex-associated renal cystogenesis.Cellular & molecular biology letters · 2024Article
- Carbonic Anhydrase 2 Deletion Delays the Growth of Kidney Cysts Whereas Foxi1 Deletion Completely Abrogates Cystogenesis in TSC.International journal of molecular sciences · 2024Article
- Pharmacological inhibition of S6K1 rescues synaptic deficits and attenuates seizures and depression in chronic epileptic rats.CNS neuroscience & therapeutics · 2024Article
- TFEB drives mTORC1 hyperactivation and kidney disease in Tuberous Sclerosis Complex.Nature communications · 2024Article
- Proteomic investigation of neural stem cell to oligodendrocyte precursor cell differentiation reveals phosphorylation-dependent Dclk1 processing.Cellular and molecular life sciences : CMLS · 2023Article
- Crosstalk between the mTOR pathway and primary cilia in human diseases.Current topics in developmental biology · 2023Review
- Primary TSC2International journal of molecular sciences · 2022Article
- LAM Cells as Potential Drivers of Senescence in Lymphangioleiomyomatosis Microenvironment.International journal of molecular sciences · 2022Article
- S6 kinase 1 at the central node of cell size and ageing.Frontiers in cell and developmental biology · 2022Review
- Insights Into Mechanisms of Oriented Division From Studies in 3D Cellular Models.Frontiers in cell and developmental biology · 2022Review
- MicroRNA-506 modulates insulin resistance in human adipocytes by targeting S6K1 and altering the IRS1/PI3K/AKT insulin signaling pathway.Journal of bioenergetics and biomembranes · 2021Article
- Spindle positioning and its impact on vertebrate tissue architecture and cell fate.Nature reviews. Molecular cell biology · 2021Review
- Cold-induction of afadin in brown fat supports its thermogenic capacity.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
mTOR activation is essential and sufficient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) and other genetic disorders. In disease models, a sharp increase of proliferation and cyst formation correlates with a dramatic loss of oriented cell division (OCD). We find that OCD distortion is intrinsically due to S6 kinase 1 (S6K1) activation. The concomitant loss of S6K1 in Tsc1-mutant mice restores OCD but does not decrease hyperproliferation, leading to non-cystic harmonious hyper growth of kidneys. Mass spectrometry-based phosphoproteomics for S6K1 substrates revealed Afadin, a known component of cell-cell junctions required to couple intercellular adhesions and cortical cues to spindle orientation. Afadin is directly phosphorylated by S6K1 and abnormally decorates the apical surface of Tsc1-mutant cells with E-cadherin and α-catenin. Our data reveal that S6K1 hyperactivity alters centrosome positioning in mitotic cells, affecting oriented cell division and promoting kidney cysts in conditions of mTOR hyperactivity.
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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.