1. GSK3β Controls mTOR and Prosurvival Signaling in Neurons.
- Author
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Urbanska M, Gozdz A, Macias M, Cymerman IA, Liszewska E, Kondratiuk I, Devijver H, Lechat B, Van Leuven F, and Jaworski J
- Subjects
- Animals, Apoptosis, Brain enzymology, Cell Differentiation, Cell Survival, Cells, Cultured, Glycogen Synthase Kinase 3 beta antagonists & inhibitors, Isoenzymes metabolism, Kainic Acid, Mice, Transgenic, Phosphorylation, Proto-Oncogene Proteins c-akt metabolism, Ribosomal Protein S6 metabolism, Glycogen Synthase Kinase 3 beta metabolism, Neurons cytology, Neurons enzymology, Signal Transduction, TOR Serine-Threonine Kinases metabolism
- Abstract
Glycogen synthase kinases-3β (GSK3β) is a key regulator of cell homeostasis. In neurons, GSK3β contributes to control of neuronal transmission and plasticity. Despite extensive studies in non-neuronal cells, crosstalk between GSK3β and other signaling pathways remains not well defined in neurons. In the present study, we report that GSK3β positively affected the activity of effectors of mammalian target of rapamycin complex 1 (mTORC1) and complex 2 (mTORC2), in mature neurons in vitro and in vivo. GSK3β also promoted prosurvival signaling and attenuated kainic acid-induced apoptosis. Our study identified GSK3β as a positive regulator of prosurvival signaling, including the mTOR pathway, and indicates the possible neuroprotective role of GSK3β in models of pharmacologically induced excitotoxicity.
- Published
- 2018
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