Protection of α-CaMKII from Dephosphorylation by GluN2B Subunit of NMDA Receptor Is Abolished by Mutation of Glu(96) or His(282) of α-CaMKII

Interaction of CaMKII and the GluN2B subunit of NMDA receptor is essential for synaptic plasticity events such as LTP. Synaptic targeting of CaMKII and regulation of its biochemical functions result from this interaction. GluN2B binding to the T-site of CaMKII leads to changes in substrate binding a...

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Detalles Bibliográficos
Autores principales: Mayadevi, Madhavan, Lakshmi, Kesavan, Suma Priya, Sudarsana Devi, John, Sebastian, Omkumar, Ramakrishnapillai V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5017783/
https://www.ncbi.nlm.nih.gov/pubmed/27610621
http://dx.doi.org/10.1371/journal.pone.0162011

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