A multi-state model of the CaMKII dodecamer suggests a role for calmodulin in maintenance of autophosphorylation
Matthew C Pharris, Neal M. Patel, Tyler G. VanDyk, Thomas M. Bartol, Terrence J. Sejnowski A B, Mary B. Kennedy, Melanie I. Stefan, Tamara L. Kinzer‐Ursem
The paper develops a rule-based computational model of CaMKII holoenzyme to explore how Ca2+/CaM binding stabilizes autophosphorylation and regulates synaptic plasticity.
PLoS Computational Biology · Dec 23, 2019Peer-reviewedNeuroscience