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

2020 ◽  
Vol 21 (19) ◽  
pp. 7272
Author(s):  
Olivier Nicole ◽  
Emilie Pacary
Keyword(s):  
Neuronal Plasticity ◽  
Neuronal Development ◽  
Brain Diseases ◽  
Dependent Protein Kinase ◽  
Potential Implication ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
The Subject ◽  
The Brain ◽  
Intense Research

The calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous and central player in Ca2+ 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 CAMK2B 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.

scholarly journals Activation State-Dependent Substrate Gating in Ca2+/Calmodulin-Dependent Protein Kinase II

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
D. E. Johnson ◽  
A. Hudmon
Keyword(s):  
Protein Kinase ◽  
Catalytic Domain ◽  
Intrinsic Property ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
State Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein ◽  
Substrate Phosphorylation ◽  
The Brain

Calcium/calmodulin-dependent protein kinase II (CaMKII) is highly concentrated in the brain where its activation by the Ca2+sensor CaM, multivalent structure, and complex autoregulatory features make it an ideal translator of Ca2+signals created by different patterns of neuronal activity. We provide direct evidence that graded levels of kinase activity and extent of T287(T286αisoform) autophosphorylation drive changes in catalytic output and substrate selectivity. The catalytic domains of CaMKII phosphorylate purified PSDs much more effectively when tethered together in the holoenzyme versus individual subunits. Using multisubstrate SPOT arrays, high-affinity substrates are preferentially phosphorylated with limited subunit activity per holoenzyme, whereas multiple subunits or maximal subunit activation is required for intermediate- and low-affinity, weak substrates, respectively. Using a monomeric form of CaMKII to control T287autophosphorylation, we demonstrate that increased Ca2+/CaM-dependent activity for all substrates tested, with the extent of weak, low-affinity substrate phosphorylation governed by the extent of T287autophosphorylation. Our data suggest T287autophosphorylation regulates substrate gating, an intrinsic property of the catalytic domain, which is amplified within the multivalent architecture of the CaMKII holoenzyme.

scholarly journals Calcium/Calmodulin–Dependent Protein Kinase II in Cerebrovascular Diseases

2021 ◽  
Author(s):  
Xuejing Zhang ◽  
Jaclyn Connelly ◽  
Edwin S. Levitan ◽  
Dandan Sun ◽  
Jane Q. Wang
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Cerebrovascular Diseases ◽  
Biological Processes ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
The Brain

AbstractCerebrovascular disease is the most common life-threatening and debilitating condition that often leads to stroke. The multifunctional calcium/calmodulin-dependent protein kinase II (CaMKII) is a key Ca2+ sensor and an important signaling protein in a variety of biological systems within the brain, heart, and vasculature. In the brain, past stroke-related studies have been mainly focused on the role of CaMKII in ischemic stroke in neurons and established CaMKII as a major mediator of neuronal cell death induced by glutamate excitotoxicity and oxidative stress following ischemic stroke. However, with growing understanding of the importance of neurovascular interactions in cerebrovascular diseases, there are clearly gaps in our understanding of how CaMKII functions in the complex neurovascular biological processes and its contributions to cerebrovascular diseases. Additionally, emerging evidence demonstrates novel regulatory mechanisms of CaMKII and potential roles of the less-studied CaMKII isoforms in the ischemic brain, which has sparked renewed interests in this dynamic kinase family. This review discusses past findings and emerging evidence on CaMKII in several major cerebrovascular dysfunctions including ischemic stroke, hemorrhagic stroke, and vascular dementia, focusing on the unique roles played by CaMKII in the underlying biological processes of neuronal cell death, neuroinflammation, and endothelial barrier dysfunction triggered by stroke. We also highlight exciting new findings, promising therapeutic agents, and future perspectives for CaMKII in cerebrovascular systems.

Calcium/Calmodulin-Dependent Protein Kinase II Involvement in Release of Gonadotropin-Releasing Hormone

1998 ◽  
Vol 67 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Wendy W. Waters ◽  
Pat L. Chen ◽  
Newell H. McArthur ◽  
Pete A. Moreno ◽  
Paul G. Harms
Keyword(s):  
Protein Kinase ◽  
Gonadotropin Releasing Hormone ◽  
Dependent Protein Kinase ◽  
Releasing Hormone ◽  
Calcium Calmodulin Dependent ◽  
Protein Kinase Ii ◽  
Dependent Protein
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