CaMKIIalpha enhances the desensitization of NR2B-containing NMDA receptors by an autophosphorylation-dependent mechanism.

@article{SessomsSikes2005CaMKIIalphaET,
  title={CaMKIIalpha enhances the desensitization of NR2B-containing NMDA receptors by an autophosphorylation-dependent mechanism.},
  author={Suzanne Sessoms-Sikes and Yumiko Honse and David M. Lovinger and Roger J Colbran},
  journal={Molecular and cellular neurosciences},
  year={2005},
  volume={29 1},
  pages={139-47}
}
Long-term potentiation or depression of synaptic function often requires Ca2+ influx via NMDA-type glutamate receptors (NMDARs) and changes in the autophosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) at Thr286. Autophosphorylated CaMKII binds directly to NMDAR subunits, co-localizes with NMDARs in the postsynaptic density, and phosphorylates NR2B subunits at Ser1303. Here, we demonstrate that CaMKIIalpha enhances the extent and/or rate of desensitization of NMDA-induced… CONTINUE READING
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