CaM-kinases: modulators of synaptic plasticity.
Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses, and studies over the past two to three years have identified key functions for Ca(2+)/calmodulin-dependent protein kinases II and IV (CaM-KII and CaM-KIV). Sustained activation of CaM-KII localized at the postsynaptic density results in phosphorylation of numerous synaptic substrates including ion channels, other signaling molecules and scaffolding proteins, to modulate synaptic transmission within minutes. More prolonged responses may be effected through enhanced dendritic protein synthesis of CaM-KII and regulation of nuclear gene transcription by CaM-KIV.
Soderling
T R
TR
Vollum Institute, L-474 Oregon Health Sciences University, Portland, OR 97201, USA. soderlit@ohsu.edu
D000818:Animals; D020013:Calcium Signaling / Q000502:physiology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000201:enzymology*
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases