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 alphaCaMKII. 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 alphaCaMKII.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
van Woerden GM,Harris KD,Hojjati MR,Gustin RM,Qiu S,de Avila Freire R,Jiang YH,Elgersma Y,Weeber EJdoi
10.1038/nn1845subject
Has Abstractpub_date
2007-03-01 00:00:00pages
280-2issue
3eissn
1097-6256issn
1546-1726pii
nn1845journal_volume
10pub_type
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journal_title:Nature neuroscience
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更新日期:2013-03-01 00:00:00
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更新日期:2010-12-01 00:00:00
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更新日期:2006-12-01 00:00:00
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更新日期:2007-12-01 00:00:00
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pub_type: 已发布勘误
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journal_title:Nature neuroscience
pub_type: 已发布勘误
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