Abstract
Angelman syndrome (AS) is a severe neurological disorder characterized by mental retardation, motor dysfunction and epilepsy. We show that the molecular and cellular deficits of an AS mouse model can be rescued by introducing an additional mutation at the inhibitory phosphorylation site of αCaMKII. Moreover, these double mutants no longer show the behavioral deficits seen in AS mice, suggesting that these deficits are the direct result of increased inhibitory phosphorylation of αCaMKII.
Original language | English (US) |
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Pages (from-to) | 280-282 |
Number of pages | 3 |
Journal | Nature neuroscience |
Volume | 10 |
Issue number | 3 |
DOIs | |
State | Published - Mar 2007 |
Externally published | Yes |
ASJC Scopus subject areas
- Neuroscience(all)