The animal model containing a E815K mutation in ATP1A3 manifests clinical and neurophysiological features of the most severe form of alternating hemiplegia of childhood.
Na(+)/K(+)-ATPase alpha3 does not reside within the core circadian molecular clockwork but Myk/+ mice exhibit concomitant disruption in circadian rhythms and mood. The Myshkin model demonstrates profound circadian and light-responsive behavioral alterations independent of molecular clock disruption.
Learning and memory deficits observed in Na K-ATPase alpha2 and alpha3 mice reveal Na K-ATPase to be an important factor in the functioning of pathways associated with spatial learning.
These data demonstrate that through its interaction with the alpha3 sodium-potassium ATPase agrin regulates activity-dependent processes in neurons providing a molecular framework for agrin action in the CNS.
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