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Enzymatic Activity of CaMKII Is Not Required for Its Interaction with the Glutamate Receptor Subunit GluN2B

Binding of the Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) to the NMDA-type glutamate receptor subunit GluN2B is an important control mechanism for the regulation of synaptic strength. CaMKII binding to GluN2B and CaMKII translocation to synapses are induced by an initial Ca(2+)/CaM...

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Bibliografske podrobnosti
Main Authors: Barcomb, Kelsey, Coultrap, Steven J., Bayer, K. Ulrich
Format: Artigo
Jezik:Inglês
Izdano: The American Society for Pharmacology and Experimental Therapeutics 2013
Teme:
Online dostop:https://ncbi.nlm.nih.gov/pmc/articles/PMC3834147/
https://ncbi.nlm.nih.gov/pubmed/24056996
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1124/mol.113.089045
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