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

First Author  van Woerden GM Year  2007
Journal  Nat Neurosci Volume  10
Issue  3 Pages  280-2
PubMed ID  17259980 Mgi Jnum  J:120721
Mgi Id  MGI:3707896 Doi  10.1038/nn1845
Citation  van Woerden GM, et al. (2007) Rescue of neurological deficits in a mouse model for Angelman syndrome by reduction of alphaCaMKII inhibitory phosphorylation. Nat Neurosci 10(3):280-2
abstractText  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.
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