CaMKIIβ in Neuronal Development and Plasticity: An Emerging Candidate in Brain Diseases

• Published in: International journal of molecular sciences 2020-10, Vol.21 (19), p.7272
• Main Authors: Nicole, Olivier, Pacary, Emilie
• Format: Article
• Language: English
• Subjects: Actin; Animals; Binding sites; brain; Brain - enzymology; Brain - physiopathology; Ca2+/calmodulin-dependent protein kinase II; Calcium ions; Calcium signalling; Calcium-binding protein; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - chemistry; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism; Calmodulin; CaMKII; Cell Movement; Cytoskeleton; Developmental plasticity; Gene Expression Regulation; Humans; Isoenzymes - chemistry; Isoenzymes - genetics; Isoenzymes - metabolism; Isoforms; Kinases; Life Sciences; Memory - physiology; Mental disorders; Mental Disorders - enzymology; Mental Disorders - genetics; Mental Disorders - physiopathology; Mutation; Neurobiology; Neurodevelopmental disorders; Neurodevelopmental Disorders - enzymology; Neurodevelopmental Disorders - genetics; Neurodevelopmental Disorders - physiopathology; neuronal development; neuronal plasticity; Neuronal Plasticity - physiology; Neurons; Neurons - enzymology; Neurons - ultrastructure; Neurons and Cognition; Neuroplasticity; Proteins; psychiatric diseases; Review; Signal Transduction; Synapses - enzymology; Synapses - ultrastructure
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21197272

The calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous and central player in Ca signaling that is best known for its functions in the brain. In particular, the α isoform of CaMKII has been the subject of intense research and it has been established as a central regulator of neuronal plasticity. In contrast, little attention has been paid to CaMKIIβ, the other predominant brain isoform that interacts directly with the actin cytoskeleton, and the functions of CaMKIIβ in this organ remain largely unexplored. However, recently, the perturbation of CaMKIIβ expression has been associated with multiple neuropsychiatric and neurodevelopmental diseases, highlighting as a gene of interest. Herein, after highlighting the main structural and expression differences between the α and β isoforms, we will review the specific functions of CaMKIIβ, as described so far, in neuronal development and plasticity, as well as its potential implication in brain diseases.