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    Nat Neurosci. 2007 Mar;10(3):280-2. Epub 2007 Jan 28.

    Rescue of neurological deficits in a mouse model for Angelman syndrome by reduction of alphaCaMKII inhibitory phosphorylation.

    van Woerden GM, Harris KD, Hojjati MR, Gustin RM, Qiu S, de Avila Freire R, Jiang YH, Elgersma Y, Weeber EJ.

    Source

    Erasmus MC, University Medical Centre, Department of Neuroscience, Dr. Molewaterplein 50, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.

    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.

    PMID:
    17259980
    [PubMed - indexed for MEDLINE]

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