Abstract
In BriefNoonan syndrome (NS) is caused by hyperactive SHP2 and is associated with cognitive deficits. Levy et al. find that NMDA receptor (NMDAR)-mediated currents are disrupted in NS and identify GluN2B Y1252 as a neural substrate of SHP2. Y1252 in turn binds the actin regulator Nck2 to control spine actin and regulate NMDAR currents.
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