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Article

Protection of α-CaMKII from Dephosphorylation by GluN2B Subunit of NMDA Receptor Is Abolished by Mutation of Glu96 or His282 of α-CaMKII.

PloS one - 1 Jan 2016

Mayadevi Madhavan, Lakshmi Kesavan, Suma Priya Sudarsana Devi, John Sebastian, Omkumar Ramakrishnapillai V

Abstract excerpt

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 and catalytic parameters and inhibition of its own dephosphorylation. We find that CaMKIINα, a natural inhibitor that...

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PMID: 27610621
DOI: 10.1371/journal.pone.0162011
PMCID: PMC5017783

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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