Inhibiting glycolysis rescues memory impairment in an intellectual disability Gdi1-null mouse

Autor: Maja Malnar, Angela Bachi, Helena H. Chowdhury, Anemari Horvat, Patrizia D’Adamo, Antonia Gurgone, Saša Trkov Bobnar, Marko Muhič, Lorenzo Piemonti, Maria Lidia Mignogna, Michela Masetti, Jelena Velebit, Veronica Bianchi, Robert Zorec, Matjaž Stenovec, Alessia Mercalli, Katja Fink, Sara Belloli, Stefano Taverna, Maja Potokar, Marko Kreft, Rosa Maria Moresco, Nina Vardjan, Maddalena Ripamonti, Umberto Restuccia

Publikováno v: Metabolism
Metabolism, clinical and experimental
116 (2021): 154463. doi:10.1016/j.metabol.2020.154463
info:cnr-pdr/source/autori:D'Adamo P.; Horvat A.; Gurgone A.; Mignogna M.L.; Bianchi V.; Masetti M.; Ripamonti M.; Taverna S.; Velebit J.; Malnar M.; Muhic M.; Fink K.; Bachi A.; Restuccia U.; Belloli S.; Moresco R.M.; Mercalli A.; Piemonti L.; Potokar M.; Bobnar S.T.; Kreft M.; Chowdhury H.H.; Stenovec M.; Vardjan N.; Zorec R./titolo:Inhibiting glycolysis rescues memory impairment in an intellectual disability Gdi1-null mouse/doi:10.1016%2Fj.metabol.2020.154463/rivista:Metabolism, clinical and experimental (Print)/anno:2021/pagina_da:154463/pagina_a:/intervallo_pagine:154463/volume:116

Objectives GDI1 gene encodes for αGDI, a protein controlling the cycling of small GTPases, reputed to orchestrate vesicle trafficking. Mutations in human GDI1 are responsible for intellectual disability (ID). In mice with ablated Gdi1, a model of ID

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c2b634b090f73e01f5e64f5a419978ac
http://europepmc.org/articles/PMC7871014