Fig. 3
From: Targeting NMDA receptors in stroke: new hope in neuroprotection
Disrupting GluN2B-DAPK1-p53 complex prevents ischemic damage. a Under ischemic condition, excitotoxic stimulation of GluN2B-containing NMDARs activate and recruit DAPK1 to the C-terminus of GluN2B. b Activated DAPK1 phosphorylate GluN2B to enhance the currents through GluN2B-containing NMDARs. On the other hand, activated DAPK1 also directly binds and phosphorylates p53 to mediate neuronal death. c Disrupting the complex by the interfering peptides protected neurons from ischemic cell death