Glycosphingolipid metabolic reprogramming drives neural differentiation

التفاصيل البيبلوغرافية
العنوان: Glycosphingolipid metabolic reprogramming drives neural differentiation
المؤلفون: Alberto Luini, Riccardo Rizzo, Salvatore Fioriniello, Vittorio Maglione, Ilaria Granata, Kei Hori, Maurizio D'Esposito, Mario Rosario Guarracino, Serena Capasso, Mikio Hoshino, Domenico Russo, Ludger Johannes, Giovanni D'Angelo, Floriana Della Ragione, Francesco Scalabrì, Eiji Sugiyama, Lucia Sticco, Mitsutoshi Setou, Gian Carlo Bellenchi, Roberto De Gregorio
المصدر: EMBO journal
37 (2017): e97674. doi:10.15252/embj.201797674
info:cnr-pdr/source/autori: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/titolo:Glycosphingolipid metabolic reprogramming drives neural differentiation/doi:10.15252%2Fembj.201797674/rivista:EMBO journal (Print)/anno:2017/pagina_da:e97674/pagina_a:/intervallo_pagine:e97674/volume:37
سنة النشر: 2017
مصطلحات موضوعية: 0301 basic medicine, Epigenomics, sialyltransferase, nervous system development, bistability, neural differentiation, Regulator, Gene Expression, nerve cell differentiation, mental disease, ganglioside, glycosphingolipid, GM3 synthase, synthetase, unclassified drug, AUTS2 protein, human, haematoside synthetase, histone, protein, sialyltransferase, Article, AUTS2 gene, epigenetics, gene, gene expression, gene function, human, lipid metabolism, lipogenesis, metabolic regulation, neuropathology, nonhuman, priority journal, promoter region, regulatory mechanism, cell differentiation, drug effect, gene silencing, genetics, HeLa cell line, metabolism, nerve cell, nuclear reprogramming, physiology, Cell Differentiation, Cellular Reprogramming, Gangliosides, Gene Silencing, Glycosphingolipids, HeLa Cells, Histones, Humans, Neurodevelopmental Disorders, Neurogenesis, Neurons, Promoter Regions, Genetic, Proteins, Sialyltransferases, AUTS2, glycosphingolipids, chemistry.chemical_compound, Gene expression, News & Views, General Neuroscience, Cell Differentiation, Glycosphingolipid, Cell biology, lipids (amino acids, peptides, and proteins), Reprogramming, Neural development, Biology, digestive system, Article, General Biochemistry, Genetics and Molecular Biology, Promoter Regions, 03 medical and health sciences, Genetic, Epigenetics, Molecular Biology, General Immunology and Microbiology, Mechanism (biology), AUTS2 protein, nutritional and metabolic diseases, carbohydrates (lipids), Cytoskeletal Proteins, 030104 developmental biology, chemistry, physiology, Function (biology), Transcription Factors
الوصف: 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 neurodevelopmental disorders in humans, indicating that glycosphingolipids are key players in this process. Nevertheless, both the molecular mechanisms that control the glycosphingolipid switch and its function in neurodevelopment are poorly understood. Here, we describe a self‐contained circuit that controls glycosphingolipid reprogramming and neural differentiation. We find that globo‐series glycosphingolipids repress the epigenetic regulator of neuronal gene expression AUTS2. AUTS2 in turn binds and activates the promoter of the first and rate‐limiting ganglioside‐producing enzyme GM3 synthase, thus fostering the synthesis of gangliosides. By this mechanism, the globo–AUTS2 axis controls glycosphingolipid reprogramming and neural gene expression during neural differentiation, which involves this circuit in neurodevelopment and its defects in neuropathology.
تدمد: 1460-2075
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::867d9fe9a818fc622d7426da594e6da0
https://pubmed.ncbi.nlm.nih.gov/29572242
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....867d9fe9a818fc622d7426da594e6da0
قاعدة البيانات: OpenAIRE