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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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| Autors principals: | , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
The American Society for Pharmacology and Experimental Therapeutics
2013
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| Matèries: | |
| Accés en línia: | 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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