Karl Ulrich Bayer

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 shows that oxygen/glucose-deprivation impairs CaMKII movement in hippocampal neurons, and inhibiting CaMKII prevents this impairment, linking it to LTP and ischemia.

This study shows that short-term CaMKII inhibition with tatCN19o does not erase existing memories and is neuroprotective in non-rodents.

The paper examines how theta-phase referenced power (tPRP) and theta-referenced phase-amplitude coupling (tPAC) change in mice during odorant discrimination learning, showing increased decoding accuracy and reduced coordination in the absence of CaMKII.

Buonarati et al. show that β-adrenergic stimulation enables LTP induction in response to LTD stimuli by switching synaptic CaMKII movement to LTP mode.

This study shows that CaMKII T286 phosphorylation is essential for both LTP and two forms of LTD, with distinct roles in synaptic movement and signaling.

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.