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mTOR referees memory and disease through mRNA repression and competition
Author(s) -
RaabGraham Kimberly F.,
Niere Farr
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12675
Subject(s) - pi3k/akt/mtor pathway , messenger rna , translation (biology) , psychological repression , rna binding protein , rna , microbiology and biotechnology , biology , chemistry , gene expression , signal transduction , genetics , gene
Mammalian target of rapamycin ( mTOR ) activity is required for memory and is dysregulated in disease. Activation of mTOR promotes protein synthesis; however, new studies are demonstrating that mTOR activity also represses the translation of mRNA s. Almost three decades ago, Kandel and colleagues hypothesised that memory was due to the induction of positive regulators and removal of negative constraints. Are these negative constraints repressed mRNA s that code for proteins that block memory formation? Herein, we will discuss the mRNA s coded by putative memory suppressors, how activation/inactivation of mTOR repress protein expression at the synapse, how mTOR activity regulates RNA binding proteins, mRNA stability, and translation, and what the possible implications of mRNA repression are to memory and neurodegenerative disorders.