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- W1990999093 abstract "Calmodulin (CaM) is a major Ca(2+) 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 Ca(2+)-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 Ca(2+), CaM, and CaMKII. The model indicates that the target-bound Ca(2+) free N-lobe has an extended lifetime and may regulate the Ca(2+) response of CaMKII during LTP induction. The model also reveals multiple kinetic pathways which have not been previously predicted for CaM-dissociation from CaMKII." @default.
- W1990999093 created "2016-06-24" @default.
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- W1990999093 date "2009-07-17" @default.
- W1990999093 modified "2023-10-06" @default.
- W1990999093 title "Dissecting cooperative calmodulin binding to CaM kinase II: a detailed stochastic model" @default.
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- W1990999093 doi "https://doi.org/10.1007/s10827-009-0173-3" @default.
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