Associated Papers
An Epilepsy-Associated GRIN2A Rare Variant Disrupts CaMKIIα Phosphorylation of GluN2A and NMDA Receptor Trafficking.
Mota Vieira M et al.
Cell Reports, 2020
The CaMKII K42M and K42R mutations are equivalent in suppressing kinase activity and targeting.
Tullis JE et al.
Plos One, 2020
Reciprocal Activation within a Kinase-Effector Complex Underlying Persistence of Structural LTP.
Saneyoshi T et al.
Neuron, 2019
De Novo Mutations in Protein Kinase Genes CAMK2A and CAMK2B Cause Intellectual Disability.
Küry S et al.
American Journal of Human Genetics, 2017
A Novel Human CAMK2A Mutation Disrupts Dendritic Morphology and Synaptic Transmission, and Causes ASD-Related Behaviors.
Stephenson JR et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2017
CaMKIIalpha enhances the desensitization of NR2B-containing NMDA receptors by an autophosphorylation-dependent mechanism.
Sessoms-Sikes S et al.
Molecular and Cellular Neurosciences, 2005
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