Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5737506 | Neuroscience | 2017 | 42 Pages |
Abstract
Mammalian/mechanistic target of rapamycin (mTOR) is a serine-threonine kinase that controls several important aspects of mammalian cell function. mTOR activity is modulated by various intra- and extracellular factors; in turn, mTOR changes rates of translation, transcription, protein degradation, cell signaling, metabolism, and cytoskeleton dynamics. mTOR has been repeatedly shown to participate in neuronal development and the proper functioning of mature neurons. Changes in mTOR activity are often observed in nervous system diseases, including genetic diseases (e.g., tuberous sclerosis complex, Pten-related syndromes, neurofibromatosis, and Fragile X syndrome), epilepsy, brain tumors, and neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, and Huntington's disease). Neuroscientists only recently began deciphering the molecular processes that are downstream of mTOR that participate in proper function of the nervous system. As a result, we are gaining knowledge about the ways in which aberrant changes in mTOR activity lead to various nervous system diseases. In this review, we provide a comprehensive view of mTOR in the nervous system, with a special focus on the neuronal functions of mTOR (e.g., control of translation, transcription, and autophagy) that likely underlie the contribution of mTOR to nervous system diseases.
Keywords
unc-51-like kinase 1HIF1αULK1RHEBp70S6K1SVZFXSEGFPKC4E-BPsCGGTSCAtg13mTORNSCBDNFMAMslong-term depressionCNS diseaseTrinucleotidelong-term potentiationLTPneuronal developmentRapamycinNeural stem cellfragile X syndromehypoxia-inducible factor 1-αepidermal growth factorBrain-derived neurotrophic factorLTDsubventricular zoneProtein kinase CNeuronal plasticityTuberous sclerosis complex
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Authors
Katarzyna Switon, Katarzyna Kotulska, Aleksandra Janusz-Kaminska, Justyna Zmorzynska, Jacek Jaworski,