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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Dades bibliogràfiques
Publicat a:PLoS One
Autors principals: Mayadevi, Madhavan, Lakshmi, Kesavan, Suma Priya, Sudarsana Devi, John, Sebastian, Omkumar, Ramakrishnapillai V.
Format: Artigo
Idioma:Inglês
Publicat: Public Library of Science 2016
Matèries:
Research Article
Accés en línia:https://ncbi.nlm.nih.gov/pmc/articles/PMC5017783/
https://ncbi.nlm.nih.gov/pubmed/27610621
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1371/journal.pone.0162011
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