Steven J. Coultrap

The paper shows that CaMKII monomers can bind GluN2B and induce synaptic potentiation, even when truncated, but only through phosphatase-resistant phosphorylation.

This study shows that CaMKII T286 autophosphorylation does not propagate at basal Ca2+ levels and is only required during the early phase of LTP induction.

The paper shows the CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding, supporting structural rather than enzymatic function in LTP.

This study compares the structure, function, and high-order assembly of neuronal CaMKII and β-isoforms using single-particle EM and biochemical methods, revealing differences in their extended states and clustering behavior.