Epsins regulate mouse embryonic stem cell exit from pluripotency and neural commitment by controlling notch activation: Stem Cells International

M Cardano, J Zasso, L Ruggiero, G Di Giacomo, M Marcatili, O Cremona, L Conti

Research output: Contribution to journalArticlepeer-review

Abstract

Epsins are part of the internalization machinery pivotal to control clathrin-mediated endocytosis. Here, we report that epsin family members are expressed in mouse embryonic stem cells (mESCs) and that epsin1/2 knockdown alters both mESC exits from pluripotency and their differentiation. Furthermore, we show that epsin1/2 knockdown compromises the correct polarization and division of mESC-derived neural progenitors and their conversion into expandable radial glia-like neural stem cells. Finally, we provide evidence that Notch signaling is impaired following epsin1/2 knockdown and that experimental restoration of Notch signaling rescues the epsin-mediated phenotypes. We conclude that epsins contribute to control mESC exit from pluripotency and allow their neural differentiation by appropriate modulation of Notch signaling. © 2019 Marina Cardano et al.
Original languageEnglish
JournalStem Cells International
Volume2019
DOIs
Publication statusPublished - 2019

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