Brain Res. 2010 Dec 17;1366:197-203. Epub 2010 Oct 1.

Calcium/calmodulin-dependent kinase II facilitated GluR6 subunit serine phosphorylation through GluR6-PSD95-CaMKII signaling module assembly in cerebral ischemia injury.

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Laboratory of Biological Cancer Therapy, Xuzhou Medical College 84 West Huai-hai Road, Xuzhou, Jiangsu, 221002 PR China.

Abstract

Although recent results suggest that GluR6 serine phosphorylation plays a prominent role in brain ischemia/reperfusion-mediated neuronal injury, little is known about the precise mechanisms regulating GluR6 receptor phosphorylation. Our present study shows that the assembly of the GluR6-PSD95-CaMKII signaling module induced by brain ischemia facilitates the serine phosphorylation of GluR6 and further induces the activation of c-Jun NH2-terminal kinase JNK. More important, a selective CaMKII inhibitor KN-93 suppressed the increase of the GluR6-PSD95-CaMKII signaling module assembly and GluR6 serine phosphorylation as well as JNK activation. Such effects were similar to be observed by NMDA receptor antagonist MK801 and L-type Ca(2+) channel (L-VGCC) blocker Nifedipine. These results demonstrate that NMDA receptors and L-VGCCs depended-CaMKII functionally modulated the phosphorylation of GluR6 via the assembly of GluR6-PSD95-CaMKII signaling module in cerebral ischemia injury.

PMID:: 20888327; [PubMed - indexed for MEDLINE]

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