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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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| Gepubliceerd in: | PLoS One |
|---|---|
| Hoofdauteurs: | , , , , |
| Formaat: | Artigo |
| Taal: | Inglês |
| Gepubliceerd in: |
Public Library of Science
2016
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| Onderwerpen: | |
| Online toegang: | 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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