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This mutation impairs splicing and cellular proliferation, albeit to a lesser extent than other SNIP1 FHA domain mutations that we identified as mediators of direct contacts with phosphorylated SF3B1

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Astrocytic K + channels and transporters facilitate the spatial buffering of extracellular K + by internalizing excess K + in regions of heightened neuronal activity and redistributing it toward less active areas via gap junction-coupled astrocytic networks