Autonomous CaMKII requires further stimulation by Ca2+/calmodulin for enhancing synaptic strength
出版年份 2014 全文链接
标题
Autonomous CaMKII requires further stimulation by Ca2+/calmodulin for enhancing synaptic strength
作者
关键词
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出版物
FASEB JOURNAL
Volume 28, Issue 8, Pages 3810-3819
出版商
FASEB
发表日期
2014-05-20
DOI
10.1096/fj.14-250407
参考文献
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注意:仅列出部分参考文献,下载原文获取全部文献信息。- Autonomous CaMKII Mediates Both LTP and LTD Using a Mechanism for Differential Substrate Site Selection
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- A Significant but Rather Mild Contribution of T286 Autophosphorylation to Ca2+/CaM-Stimulated CaMKII Activity
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- Nucleotides and Phosphorylation Bi-directionally Modulate Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII) Binding to theN-Methyl-d-aspartate (NMDA) Receptor Subunit GluN2B
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- Effective Post-insult Neuroprotection by a Novel Ca2+/ Calmodulin-dependent Protein Kinase II (CaMKII) Inhibitor
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- CaMKII "Autonomy" Is Required for Initiating But Not for Maintaining Neuronal Long-Term Information Storage
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- Autonomous CaMKII Can Promote either Long-Term Potentiation or Long-Term Depression, Depending on the State of T305/T306 Phosphorylation
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- Selective translocation of Ca2+/calmodulin protein kinase II (CaMKII ) to inhibitory synapses
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- Regulation of Postsynaptic Structure and Function by an A-Kinase Anchoring Protein-Membrane-Associated Guanylate Kinase Scaffolding Complex
- (2009) H. R. Robertson et al. JOURNAL OF NEUROSCIENCE
- Activation of CaMKII in single dendritic spines during long-term potentiation
- (2009) Seok-Jin R. Lee et al. NATURE
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