GRIN2A and Angelman syndrome: Several trisomic proteins that were upregulated in trisomic mice included members of protein families that deal with vesicle exocytosis (Rab5B), synaptic signaling (FMR1), synaptic elimination (UBE3A; recent evidence supports the role of UBE3A in excessive synaptic elimination in Angelman’s syndrome and autism [49]), ER-PSD transport (MYO5A), PSD cytoskeleton (DBN1), a-synuclein transport (MYO1D), and NMDA receptor activity (GRIN2A).