Glycosphingolipid metabolic reprogramming drives neural differentiation

Neural development is accomplished by differentiation events leading to metabolic reprogramming. Glycosphingolipid metabolism is reprogrammed during neural development with a switch from globo‐ to ganglio‐series glycosphingolipid production. Failure to execute this glycosphingolipid switch leads to...

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Bibliographic Details
Published in:	The EMBO journal Vol. 37; no. 7
Main Authors:	Russo, Domenico, Della Ragione, Floriana, Rizzo, Riccardo, Sugiyama, Eiji, Scalabrì, Francesco, Hori, Kei, Capasso, Serena, Sticco, Lucia, Fioriniello, Salvatore, De Gregorio, Roberto, Granata, Ilaria, Guarracino, Mario R, Maglione, Vittorio, Johannes, Ludger, Bellenchi, Gian Carlo, Hoshino, Mikio, Setou, Mitsutoshi, D'Esposito, Maurizio, Luini, Alberto, D'Angelo, Giovanni
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 03.04.2018 Springer Nature B.V EMBO Press John Wiley and Sons Inc
Subjects:	Acetylation AUTS2 bistability Cell differentiation Cell Differentiation - drug effects Cell Differentiation - genetics Cell Differentiation - physiology Cellular Reprogramming - drug effects Cellular Reprogramming - physiology Circuits Constraining Cytoskeletal Proteins Differentiation (biology) EMBO21 EMBO27 Enzymes epigenetics Epigenomics Gangliosides Gangliosides - metabolism Gene Expression Gene Silencing Glycosphingolipids Glycosphingolipids - metabolism Glycosphingolipids - pharmacology HeLa Cells Histones - metabolism Humans Lactosylceramide a-2,3-sialyltransferase Life Sciences Metabolism Molecular modelling neural differentiation Neural stem cells Neurodevelopmental Disorders Neurogenesis - drug effects Neurogenesis - genetics Neurogenesis - physiology Neurons - metabolism Promoter Regions, Genetic - drug effects Proteins - genetics Proteins - metabolism Sialyltransferases - genetics Sialyltransferases - metabolism Stem cells Transcription Factors bistability AUTS2 neural differentiation epigenetics glycosphingolipids
ISSN:	0261-4189, 1460-2075, 1460-2075
Online Access:	Get full text
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