Fast Decay of CaMKII FRET Sensor Signal in Spines after LTP Induction Is Not Due to Its Dephosphorylation. - sprookjes - yvandenbroek - TriplyDB

Fast Decay of CaMKII FRET Sensor Signal in Spines after LTP Induction Is Not Due to Its Dephosphorylation.

Fast Decay of CaMKII FRET Sensor Signal in Spines after LTP Induction Is Not Due to Its Dephosphorylation.

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Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca2+ Signals during LTP Induction, but Not Maintenance.Interplay of enzymatic and structural functions of CaMKII in long-term potentiation.Memory Erasure Experiments Indicate a Critical Role of CaMKII in Memory Storage.CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence.Physiological and Pathological Roles of CaMKII-PP1 Signaling in the Brain.Memories of John Lisman.

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P2860

Fast Decay of CaMKII FRET Sensor Signal in Spines after LTP Induction Is Not Due to Its Dephosphorylation.

http://www.wikidata.org/entity/Q30384588

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2015 թվականի հունիսին հրատարակված գիտական հոդված

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2015年の論文

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2015年學術文章

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name

Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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Fast Decay of CaMKII FRET Sens ...... Due to Its Dephosphorylation.

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John E Lisman

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Nikolai Otmakhov

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Shaurav Regmi

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P2860

A synaptic model of memory: long-term potentiation in the hippocampus

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

Mechanisms of CaMKII action in long-term potentiation

Differential effects of phosphatase inhibitors on the calcium homeostasis and migration of HaCaT keratinocytes

A Mechanism for Tunable Autoinhibition in the Structure of a Human Ca2+/Calmodulin- Dependent Kinase II Holoenzyme

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

Dendritic spine geometry is critical for AMPA receptor expression in hippocampal CA1 pyramidal neurons

Excitotoxic insult results in a long-lasting activation of CaMKIIα and mitochondrial damage in living hippocampal neurons

Learning induces long-term potentiation in the hippocampus

CaMKII autonomy is substrate-dependent and further stimulated by Ca2+/calmodulin.

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