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Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation.
Induction of LTP increased the phosphorus-32 labeling of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA-Rs), which mediate rapid excitatory synaptic transmission and provides a postsynaptic molecular mechanism for synaptic plasticity.
Ca2+/calmodulin-kinase II enhances channel conductance of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate type glutamate receptors.
Results indicate that CaM-KII can mediate plasticity at glutamatergic synapses by increasing single-channel conductance of existing functional AMPA-Rs or by recruiting new high-conductance-state AMPA -Rs.
Extrasynaptic Membrane Trafficking Regulated by GluR1 Serine 845 Phosphorylation Primes AMPA Receptors for Long-term Potentiation*
A two-step model for delivery of GluR1-containing AM PARs to synapses during activity-dependent LTP is supported, where Ser-845 phosphorylation can traffic AMPARs to extrasynaptic sites for subsequent delivery tosynapses during LTP.
Identification of the Ca2+/Calmodulin-dependent Protein Kinase II Regulatory Phosphorylation Site in the α-Amino-3-hydroxyl-5-methyl4-isoxazole-propionate-type Glutamate Receptor*
The Ser831 site is specific to GluR1, and CaM-KII did not phosphorylate or potentiate current in cells expressing GluGluR2, emphasizing the importance of the GLUR1 subunit in this regulatory mechanism.
Regulatory mechanisms of AMPA receptors in synaptic plasticity
Recent evidence that alterations to AMPAR functional properties are coupled to their trafficking, cytoskeletal dynamics and local protein synthesis offer new insights into the regulation of AMPARs and synaptic strength by cellular signalling is focused on.
Calcium promotes cell survival through CaM-K kinase activation of the protein-kinase-B pathway
A Ca2+/calmodulin-dependent protein kinase kinase (CaM-KK) activates PKB directly, resulting in phosphorylation of BAD on serine residue 136 and the interaction of BAD with protein 14-3-3, which protects cells from apoptosis.
Postsynaptic protein phosphorylation and LTP
Characterization of a calmodulin kinase II inhibitor protein in brain.
The results characterize a potent and specific cellular inhibitor of CaM-KII that may have an important role in the physiological regulation of this key protein kinase.
An activity-regulated microRNA controls dendritic plasticity by down-regulating p250GAP
It is shown that microRNA 132 (miR132) is an activity-dependent rapid response gene regulated by the cAMP response element-binding (CREB) protein pathway and proposed that the miR132–p250GAP pathway plays a key role in activity- dependent structural and functional plasticity.