The CaMKII K42M and K42R mutations are equivalent in suppressing kinase activity and targeting.

摘要: CaMKII is an important mediator of forms synaptic plasticity that are thought to underly learning and memory. The mutants K42M K42R have been used interchangeably as research tools, although some reported phenotypic differences suggest they may differ in the extent which impair ATP binding. Here, we directly compared two mutations at high concentrations exist within cells (~4 mM). We found both equally blocked GluA1 phosphorylation vitro GluN2B binding cells. Both also reduced but did not completely abolish T286 autophosphorylation or movement excitatory synapses neurons. Thus, despite previously suggested differences, appear interfere with same extent.