Src kinases: a hub for NMDA receptor regulation

By Michael W. Salter, Lorraine V. Kalia. Nature Reviews Neuroscience, 2004

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Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease (2011, background): “At postsynaptic sites, FYN phosphorylates the NMDAR subunit 2B (NR2B), thereby mediating complex formation of NMDARs with the postsynaptic density protein 95 (PSD95”
Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. (2007, positive): “…in glutamate receptors, we examined the phosphorylation state of tyrosine residue 1472 of the NR2B subunit of NMDARs, which modulates calcium conductance, is associated with long-term potentiation (LTP) induction, and controls internalization of the receptor (reviewed in Salter and Kalia, 2004).”
Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, positive): “through activation of nonreceptor tyrosine kinases such as Src or Fyn.(42,106,107,268) Stimulation of AMPAR and group I mGluRs(89,106,118,281)”
Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models. (2010, positive): “Fyn phosphorylates the NR subunit 2 (NR2) to facilitate interaction of the NR complex with the postsynaptic density protein 95 (PSD-95) (Nakazawa et al., 2001; Rong et al., 2001; Tezuka et al., 1999), linking NRs to synaptic excitotoxic downstream signaling (Salter and Kalia, 2004).”