Associated Papers
Structural dynamics of mixed-subunit CaMKIIα/β heterododecamers filmed by high-speed AFM.
Matsushima K et al.
Nature Communications, 2025
Discriminating activating, deactivating and resistance variants in protein kinases.
Singh G et al.
Genome Medicine, 2025
Degradation of CaMKII is stimulated by its active conformation.
Quasney C et al.
The Journal of Biological Chemistry, 2025
The CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding.
Larsen ME et al.
Biorxiv : the Preprint Server for Biology, 2025
Osteoblast-lineage calcium/calmodulin-dependent kinase 2 delta and gamma regulates bone mass and quality.
Leser JM et al.
Proceedings of the National Academy of Sciences of the United States of America, 2023
Deletion of the Neuronal Transcription Factor Satb1 Induced Disturbance of the Kinome and Mechanisms of Hypoxic Preconditioning.
Turovsky EA et al.
Biology, 2023
Molecular basis of interactions between CaMKII and α-actinin-2 that underlie dendritic spine enlargement.
Curtis AJ et al.
Elife, 2023
Förster resonance energy transfer-based kinase mutation phenotyping reveals an aberrant facilitation of Ca2+/calmodulin-dependent CaMKIIα activity in de novo mutations related to intellectual disability.
Fujii H et al.
Frontiers in Molecular Neuroscience, 2022
PDSS1-Mediated Activation of CAMK2A-STAT3 Signaling Promotes Metastasis in Triple-Negative Breast Cancer.
Yu TJ et al.
Cancer Research, 2021
Characterization of six CaMKIIα variants found in patients with schizophrenia.
Brown CN et al.
Iscience, 2021
Functional implications of CaMKII alternative splicing.
Sloutsky R et al.
The European Journal of Neuroscience, 2021
Role of Satb1 and Satb2 Transcription Factors in the Glutamate Receptors Expression and Ca2+ Signaling in the Cortical Neurons In Vitro.
Turovsky EA et al.
International Journal of Molecular Sciences, 2021
Locally-Induced CaMKII Translocation Requires Nucleotide Binding.
Fitzgerald ZT et al.
Frontiers in Synaptic Neuroscience, 2020
CAMK2-Dependent Signaling in Neurons Is Essential for Survival.
Kool MJ et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2019
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
Quantitative proteomics analysis of CaMKII phosphorylation and the CaMKII interactome in the mouse forebrain.
Baucum AJ et al.
Acs Chemical Neuroscience, 2015
αCaMKII controls the establishment of cocaine's reinforcing effects in mice and humans.
Easton AC et al.
Translational Psychiatry, 2014
Loss of Thr286 phosphorylation disrupts synaptic CaMKIIα targeting, NMDAR activity and behavior in pre-adolescent mice.
Gustin RM et al.
Molecular and Cellular Neurosciences, 2011
Structure of the CaMKIIdelta/calmodulin complex reveals the molecular mechanism of CaMKII kinase activation.
Rellos P et al.
Plos Biology, 2010
Ca2+-dependent facilitation of Cav1.3 Ca2+ channels by densin and Ca2+/calmodulin-dependent protein kinase II.
Jenkins MA et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2010
CaMKIIalpha enhances the desensitization of NR2B-containing NMDA receptors by an autophosphorylation-dependent mechanism.
Sessoms-Sikes S et al.
Molecular and Cellular Neurosciences, 2005