ArticleStem cell reports2019
Clathrin-Mediated Endocytosis Regulates a Balance between Opposing Signals to Maintain the Pluripotent State of Embryonic Stem Cells.
Article in Stem cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Pathogenic mutations in clathrin heavy chain disrupt synapse architecture and learning iniScience · 2026Article
- Elevated endocytic trafficking mediated by GPRASP2 maintains HSC fidelity.bioRxiv : the preprint server for biology · 2026Article
- Microplastics promote chemoresistance by mediating lipid metabolism and suppressing pyroptosis in colorectal cancer.Apoptosis : an international journal on programmed cell death · 2025Article
- Transcriptomic and proteomic analyses of SH-SY5Y neuroblastoma cells treated with amisulpride.Acta neuropsychiatrica · 2025Article
- CLCa mediates a novel cross-talk between Wnt secretion and actin organization.Life science alliance · 2025Article
- Don't be so naïve.eLife · 2024Article
- Article
- The AP-2 complex interacts with γ-TuRC and regulates the proliferative capacity of neural progenitors.Life science alliance · 2024Article
- Understanding the interplay of membrane trafficking, cell surface mechanics, and stem cell differentiation.Seminars in cell & developmental biology · 2023Review
- Cell-cell adhesions in embryonic stem cells regulate the stability and transcriptional activity of β-catenin.FEBS letters · 2022Article
- Sterols lower energetic barriers of membrane bending and fission necessary for efficient clathrin-mediated endocytosis.Cell reports · 2021Article
- Deregulation of CLTC interacts with TFG, facilitating osteosarcoma via the TGF-beta and AKT/mTOR signaling pathways.Clinical and translational medicine · 2021Article
- Mechanical force-driven TNFα endocytosis governs stem cell homeostasis.Bone research · 2021Article
- Clathrin Light Chains: Not to Be Taken so Lightly.Frontiers in cell and developmental biology · 2021Review
- Cyclodextrin-Based Nanostructure Efficiently Delivers siRNA to Glioblastoma Cells Preferentially via Macropinocytosis.International journal of molecular sciences · 2020Article
- Pluripotency of embryonic stem cells lacking clathrin-mediated endocytosis cannot be rescued by restoring cellular stiffness.The Journal of biological chemistry · 2020Article
- MicroRNA-dependent inhibition of PFN2 orchestrates ERK activation and pluripotent state transitions by regulating endocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Endocytosis is implicated in the maintenance of embryonic stem cell (ESC) pluripotency, although its exact role and the identity of molecular players remain poorly understood. Here, we show that the clathrin heavy chain (CLTC), involved in clathrin-mediated endocytosis (CME), is vital for maintaining mouse ESC (mESC) pluripotency. Knockdown of Cltc resulted in a loss of pluripotency accompanied by reduced E-cadherin (E-CAD) levels and increased levels of transforming growth factor β (TGF-β) and extracellular signal-regulated kinase (ERK) signaling. We demonstrate that both E-CAD and TGF-β receptor type 1 (TGF-βR1) are internalized through CME in mESCs. While E-CAD is recycled, TGF-βR1 is targeted for lysosomal degradation thus maintaining inverse levels of these molecules. Finally, we show that E-CAD interacts with ERK, and that the decreased pluripotency upon CME loss can be rescued by inhibiting TGF-βR, MEK, and GSK3β, or overexpressing E-CAD. Our results demonstrate that CME is critical for balancing signaling outputs to regulate ESC pluripotency, and possibly cell fate choices in early development.
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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.