Angelman Syndrome: Finding the Lost Arc

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Angelman Syndrome: Finding the Lost Arc Hwan-Ching Tai, Erin M. Schuman Cell Volume 140, Issue 5, Pages 608-610 (March 2010) DOI: 10.1016/j.cell.2010.02.019 Copyright © 2010 Elsevier Inc. Terms and Conditions

Figure 1 UBE3A, Arc, and AMPAR Endocytosis Mutations in the UBE3A gene, which encodes an E3 ubiquitin ligase, are a cause of a neurodevelopmental disorder called Angelman syndrome. (Left) A substrate of UBE3A in synapses, Arc, is transcribed rapidly after robust neuronal stimulation and promotes the internalization of AMPA-type glutamate receptors (AMPARs), resulting in a reduction in synaptic strength. (Middle) Several hours after neuronal stimulation, newly synthesized UBE3A ubiquitinates Arc to promote its degradation by the proteasome, thus preventing further internalization of AMPARs. (Right) A disruption in the function of UBE3A in neurons leads to increased expression of Arc and a decrease in AMPARs at excitatory synapses, which may contribute to the neurological symptoms of Angelman syndrome. Cell 2010 140, 608-610DOI: (10.1016/j.cell.2010.02.019) Copyright © 2010 Elsevier Inc. Terms and Conditions