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- W63611256 abstract "Angelman syndrome (AS) is a disorder of maternal imprinting and disrupted ubiquitin ligase function characterized by severe mental retardation and epilepsy. A mouse model for AS was developed that displays similar molecular and behavioral phenotypes to the human condition. Interestingly, neither the mouse model nor human AS patients display detectable neuroanatomical defects, suggesting that disruption of cognitive function in AS is due to altered synaptic plasticity or cellular signaling. At a molecular level, AS mice exhibit a significant increase in hippocampal phospho-calcium/calmodulin-dependent protein kinase II (CaMKII), specifically at sites Thr(286) and Thr(305). Importantly, the major phenotypes of the AS mouse can be rescued with the addition of mutations at the Thr(305) phosphorylation site. This chapter explores the implications of CaMKII misregulation as a molecular cause for the neurobehavioral deficits in AS and the potential mechanisms underlying CaMKII dysfunction in Angelman syndrome." @default.
- W63611256 created "2016-06-24" @default.
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- W63611256 date "2008-01-01" @default.
- W63611256 modified "2023-09-23" @default.
- W63611256 title "Angelman Syndrome" @default.
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- W63611256 doi "https://doi.org/10.1016/b978-012370509-9.00027-9" @default.
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