TY - JOUR
T1 - CaM-kinases
T2 - Modulators of synaptic plasticity
AU - Soderling, Thomas R.
PY - 2000/6/1
Y1 - 2000/6/1
N2 - 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 Ca2+/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.
AB - 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 Ca2+/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.
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U2 - 10.1016/S0959-4388(00)00090-8
DO - 10.1016/S0959-4388(00)00090-8
M3 - Review article
C2 - 10851169
AN - SCOPUS:0034043203
SN - 0959-4388
VL - 10
SP - 375
EP - 380
JO - Current Opinion in Neurobiology
JF - Current Opinion in Neurobiology
IS - 3
ER -