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• W2022783417 startingPage "1459" @default.
• W2022783417 abstract "Dendritic protein homeostasis is crucial for most forms of long-term synaptic plasticity, and its dysregulation is linked to a wide range of brain disorders. Current models of metabotropic glutamate receptor mediated long-term depression (mGluR-LTD) suggest that rapid, local synthesis of key proteins is necessary for the induction and expression of LTD. Here, we find that mGluR-LTD can be induced in the absence of translation if the proteasome is concurrently inhibited. We report that enhanced proteasomal degradation during the expression of mGluR-LTD depletes dendritic proteins and inhibits subsequent inductions of LTD. Moreover, proteasome inhibition can rescue mGluR-LTD in mice null for the RNA binding protein Sam68, which we show here lack mGluR-dependent translation and LTD. Our study provides mechanistic insights for how changes in dendritic protein abundance regulate mGluR-LTD induction. We propose that Sam68-mediated translation helps to counterbalance degradation, ensuring that protein levels briefly remain above a permissive threshold during LTD induction." @default.
• W2022783417 created "2016-06-24" @default.
• W2022783417 creator A5003155578 @default.
• W2022783417 creator A5012013975 @default.
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• W2022783417 date "2015-03-01" @default.
• W2022783417 modified "2023-10-02" @default.
• W2022783417 title "Coordination between Translation and Degradation Regulates Inducibility of mGluR-LTD" @default.
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• W2022783417 doi "https://doi.org/10.1016/j.celrep.2015.02.020" @default.
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