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Journal of Computational Neuroscience

Erschienen in:

01.12.2009

Dissecting cooperative calmodulin binding to CaM kinase II: a detailed stochastic model

verfasst von: Michael J. Byrne, John A. Putkey, M. Neal Waxham, Yoshihisa Kubota

Erschienen in: Journal of Computational Neuroscience | Ausgabe 3/2009

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Abstract

Calmodulin (CaM) is a major Ca²⁺ binding protein involved in two opposing processes of synaptic plasticity of CA1 pyramidal neurons: long-term potentiation (LTP) and depression (LTD). The N- and C-terminal lobes of CaM bind to its target separately but cooperatively and introduce complex dynamics that cannot be well understood by experimental measurement. Using a detailed stochastic model constructed upon experimental data, we have studied the interaction between CaM and Ca²⁺-CaM-dependent protein kinase II (CaMKII), a key enzyme underlying LTP. The model suggests that the accelerated binding of one lobe of CaM to CaMKII, when the opposing lobe is already bound to CaMKII, is a critical determinant of the cooperative interaction between Ca²⁺, CaM, and CaMKII. The model indicates that the target-bound Ca²⁺ free N-lobe has an extended lifetime and may regulate the Ca²⁺ response of CaMKII during LTP induction. The model also reveals multiple kinetic pathways which have not been previously predicted for CaM-dissociation from CaMKII.

Vorheriger Artikel Recurrent networks with short term synaptic depression

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Titel: Dissecting cooperative calmodulin binding to CaM kinase II: a detailed stochastic model
verfasst von: Michael J. Byrne
John A. Putkey
M. Neal Waxham
Yoshihisa Kubota
Publikationsdatum: 01.12.2009
Verlag: Springer US
Erschienen in: Journal of Computational Neuroscience / Ausgabe 3/2009
Print ISSN: 0929-5313
Elektronische ISSN: 1573-6873
DOI: https://doi.org/10.1007/s10827-009-0173-3

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