A model of the roles of essential kinases in the induction and expression of late long-term potentiation. - Wikidata - awgldk - TriplyDB

A model of the roles of essential kinases in the induction and expression of late long-term potentiation.

A model of the roles of essential kinases in the induction and expression of late long-term potentiation.

http://www.wikidata.org/entity/Q34481520

about

Calmodulin-kinases: modulators of neuronal development and plasticity The right time to learn: mechanisms and optimization of spaced learning A model of late long-term potentiation simulates aspects of memory maintenance Gene expression in human hippocampus from cocaine abusers identifies genes which regulate extracellular matrix remodeling Synaptic input sequence discrimination on behavioral timescales mediated by reaction-diffusion chemistry in dendrites.A new principle for information storage in an enzymatic pathway model.Tag-trigger-consolidation: a model of early and late long-term-potentiation and depression STEPS: Modeling and Simulating Complex Reaction-Diffusion Systems with Python.Molecular constraints on synaptic tagging and maintenance of long-term potentiation: a predictive model.Coupling of metabolic, second messenger pathways and insulin granule dynamics in pancreatic beta-cells: a computational analysis Pancreatic Beta Cell G-Protein Coupled Receptors and Second Messenger Interactions: A Systems Biology Computational Analysis Nicotinic Acetylcholine Receptors Sensitize a MAPK-linked Toxicity Pathway on Prolonged Exposure to β-Amyloid.Linking Memories across Time via Neuronal and Dendritic Overlaps in Model Neurons with Active Dendrites The Contribution of Spatial and Temporal Molecular Networks in the Induction of Long-term Memory and Its Underlying Synaptic Plasticity Postsynaptic signal transduction models for long-term potentiation and depression.The effects of cascade length, kinetics and feedback loops on biological signal transduction dynamics in a simplified cascade model.Simulations suggest pharmacological methods for rescuing long-term potentiation.Translational switch for long-term maintenance of synaptic plasticity.Deficit in long-term synaptic plasticity is rescued by a computationally predicted stimulus protocol.Bistable MAP kinase activity: a plausible mechanism contributing to maintenance of late long-term potentiation.AMPA receptor trafficking and its role in heterosynaptic plasticity.FindSim: A Framework for Integrating Neuronal Data and Signaling Models.

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P2860

A model of the roles of essential kinases in the induction and expression of late long-term potentiation.

http://www.wikidata.org/entity/Q34481520

description

2006 nî lūn-bûn

@nan

2006 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2006 թվականի հունվարին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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type

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A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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A model of the roles of essent ...... f late long-term potentiation.

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BIOPHYSJ.105.072470

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Biophysical Journal

P1476

A model of the roles of essent ...... f late long-term potentiation.

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Douglas A Baxter

http://www.w3.org/2001/XMLSchema#string

John H Byrne

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Paul Smolen

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P2860

A family of cAMP-binding proteins that directly activate Rap1

Long-Term Potentiation and Memory

Noise in gene expression: origins, consequences, and control.

Ultrasensitivity in the mitogen-activated protein kinase cascade

Time-restricted role for dendritic activation of the mTOR-p70S6K pathway in the induction of late-phase long-term potentiation in the CA1

Rolipram, a type IV-specific phosphodiesterase inhibitor, facilitates the establishment of long-lasting long-term potentiation and improves memory

An ultrasensitive Ca2+/calmodulin-dependent protein kinase II-protein phosphatase 1 switch facilitates specificity in postsynaptic calcium signaling

Molecular switches at the synapse emerge from receptor and kinase traffic

Protein kinase M zeta synthesis from a brain mRNA encoding an independent protein kinase C zeta catalytic domain. Implications for the molecular mechanism of memory

Phosphatidylinositol 3-kinase is required for the expression but not for the induction or the maintenance of long-term potentiation in the hippocampal CA1 region

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2760-2775

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scholarly article

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10.1529/BIOPHYSJ.105.072470

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8

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16415049

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q-bio/0601004

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1414565

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