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Título:	Proteasomal-mediated degradation of AKAP150 accompanies AMPAR endocytosis during cLTD
Autor/a:	Cheng, Wenwen; Siedlecki-Wullich, Dolores; Català-Solsona, Judit; Fábregas, Cristina; Fadó Andrés, Rut; Casals i Farré, Núria; Solé, Montse; Unzeta, Mercedes; Saura, Carlos A.; Rodríguez-Álvarez, José; Miñano Molina, Alfredo Jesús
Notas:	The number and function of synaptic AMPA receptors (AMPARs) tightly regulates excitatory synaptic transmission. Current evidence suggests that AMPARs are inserted into the postsynaptic membrane during long-term potentiation (LTP) and are removed from the membrane during long-term depression (LTD). Dephosphorylation of GluA1 at Ser-845 and enhanced endocytosis are critical events in the modulation of LTD. Moreover, changes in scaffold proteins from the postsynaptic density (PSD) could be also related to AMPAR regulation in LTD. In the present study we analyzed the effect of chemical LTD (cLTD) on A-kinase anchoring protein (AKAP)150 and AMPARs levels in mouse-cultured neurons. We show that cLTD induces AKAP150 protein degradation via proteasome, coinciding with GluA1 dephosphorylation at Ser-845 and endocytosis of GluA1-containing AMPARs. Pharmacological inhibition of proteasome activity, but not phosphatase calcineurin (CaN), reverted cLTD-induced AKAP150 protein degradation. Importantly, AKAP150 silencing induced dephosphorylation of GluA1 Ser-845 and GluA1-AMPARs endocytosis while AKAP150 overexpression blocked cLTD-mediated GluA1-AMPARs endocytosis. Our results provide direct evidence that cLTD-induced AKAP150 degradation by the proteasome contributes to synaptic AMPARs endocytosis.
Materia(s):	-Sistema nerviós -- Degeneració -Trastorns de la memòria -Neurobiologia -Proteïnes -Immunocitoquímica -Sistema nervioso -- Degeneración -Memoria -- Trastornos -Neurobiología -Proteínas -Inmunocitoquímica -Nervous system -- Degeneration -Memory disorders -Neurobiology -Proteins -Immunocytochemistry -616.3
Derechos:	© 2020 Cheng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. https://creativecommons.org/licenses/by/4.0/
Tipo de documento:	Artículo Artículo - Versión aceptada
Editor:	Society for Neuroscience
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