Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength - Wikidata - awgldk - TriplyDB

Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

http://www.wikidata.org/entity/Q35111818

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Mechanisms of CaMKII action in long-term potentiation The synaptic maintenance problem: membrane recycling, Ca2+ homeostasis and late onset degeneration Ultrastructural abnormalities in CA1 hippocampus caused by deletion of the actin regulator WAVE-1 Improving a natural CaMKII inhibitor by random and rational design CaMKII binding to GluN2B is critical during memory consolidation Excitotoxic insult results in a long-lasting activation of CaMKIIα and mitochondrial damage in living hippocampal neurons Protection of α-CaMKII from Dephosphorylation by GluN2B Subunit of NMDA Receptor Is Abolished by Mutation of Glu96 or His282 of α-CaMKII Surface dynamics of GluN2B-NMDA receptors controls plasticity of maturing glutamate synapses SorCS2-mediated NR2A trafficking regulates motor deficits in Huntington's disease Fast Decay of CaMKII FRET Sensor Signal in Spines after LTP Induction Is Not Due to Its Dephosphorylation.Reduced synaptic STIM2 expression and impaired store-operated calcium entry cause destabilization of mature spines in mutant presenilin mice.A significant but rather mild contribution of T286 autophosphorylation to Ca2+/CaM-stimulated CaMKII activity.Molecular constraints on synaptic tagging and maintenance of long-term potentiation: a predictive model.Effect of multimeric structure of CaMKII in the GluN2B-mediated modulation of kinetic parameters of ATP.Genetic inhibition of CaMKII in dorsal striatal medium spiny neurons reduces functional excitatory synapses and enhances intrinsic excitability.On the mechanism of synaptic depression induced by CaMKIIN, an endogenous inhibitor of CaMKII.The initiation of synaptic 2-AG mobilization requires both an increased supply of diacylglycerol precursor and increased postsynaptic calcium.Efficacy of lovastatin on learning and memory deficits caused by chronic intermittent hypoxia-hypercapnia: through regulation of NR2B-containing NMDA receptor-ERK pathway.Nucleotides and phosphorylation bi-directionally modulate Ca2+/calmodulin-dependent protein kinase II (CaMKII) binding to the N-methyl-D-aspartate (NMDA) receptor subunit GluN2B.Kinetic memory based on the enzyme-limited competition Catalytically Dead αCaMKII K42M Mutant Acts as a Dominant Negative in the Control of Synaptic Strength.Activity-dependent regulation of synaptic strength by PSD-95 in CA1 neurons Substrate-selective and calcium-independent activation of CaMKII by α-actinin.Bi-directional regulation of CaMKIIα phosphorylation at Thr286 by NMDA receptors in cultured cortical neurons Possible Signaling Pathways Mediating Neuronal Calcium Sensor-1-Dependent Spatial Learning and Memory in Mice CaMKII regulation in information processing and storage.Coordination of Protein Phosphorylation and Dephosphorylation in Synaptic Plasticity Diversity in NMDA receptor composition: many regulators, many consequences.The CaMKII/NMDAR complex as a molecular memory Activated CaMKII couples GluN2B and casein kinase 2 to control synaptic NMDA receptors.Persistent reversal of enhanced amphetamine intake by transient CaMKII inhibition The delicate bistability of CaMKII Phosphoproteomic Analysis Reveals a Novel Mechanism of CaMKIIα Regulation Inversely Induced by Cocaine Memory Extinction versus Reconsolidation Cdk5 Modulates Long-Term Synaptic Plasticity and Motor Learning in Dorsolateral Striatum Recombinant probes reveal dynamic localization of CaMKIIα within somata of cortical neurons.Enzymatic activity of CaMKII is not required for its interaction with the glutamate receptor subunit GluN2B.Hippocampal long-term potentiation is disrupted during expression and extinction but is restored after reinstatement of morphine place preference.Activation-triggered subunit exchange between CaMKII holoenzymes facilitates the spread of kinase activity Refreshing memories.CaMKII activity in the ventral tegmental area gates cocaine-induced synaptic plasticity in the nucleus accumbens.

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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2011年の論文

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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JNEUROSCI.1250-11.2011

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Journal of Neuroscience

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Role of the CaMKII/NMDA receptor complex in the maintenance of synaptic strength

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German Fernandez-Villalobos

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Gyulnara Kasumova

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Ivar S Stein

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Johannes W Hell

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John Lisman

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K Ulrich Bayer

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Magdalena Sanhueza

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Nikolai Otmakhov

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Peng Zhang

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Optical induction of plasticity at single synapses reveals input-specific accumulation of alphaCaMKII

Characterization of a calmodulin kinase II inhibitor protein in brain

Activation of CaMKII in single dendritic spines during long-term potentiation

Densin-180 forms a ternary complex with the (alpha)-subunit of Ca2+/calmodulin-dependent protein kinase II and (alpha)-actinin

Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice

The molecular basis of CaMKII function in synaptic and behavioural memory

Translocation of autophosphorylated calcium/calmodulin-dependent protein kinase II to the postsynaptic density

Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning

SynGAP-MUPP1-CaMKII synaptic complexes regulate p38 MAP kinase activity and NMDA receptor-dependent synaptic AMPA receptor potentiation

Reversal of synaptic memory by Ca2+/calmodulin-dependent protein kinase II inhibitor

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9170-9178

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10.1523/JNEUROSCI.1250-11.2011

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51242383

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21697368

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