A-Kinase Anchoring Proteins (AKAPs) ensure the fidelity of second messenger signaling events by directing protein kinases and phosphatases toward their preferred substrates. AKAP150 (Akap5, A kinase (PRKA) anchor protein 5) brings protein kinase A (PKA), the calcium/calmodulin dependent phosphatase PP2B and protein kinase C (PKC) to postsynaptic membranes where they facilitate the phosphorylation dependent modulation of certain ion channels.

Exon 2 of the mouse Akap5 gene has been deleted to create a knockout allele in these targeted mutant mice. Homozygous mice have impaired motor coordination and strength, harbor deficits in spatial memory retention, and show reduced anxiety. Loss of AKAP5 in sympathetic cervical ganglion (SCG) neurons reduces muscarinic suppression of inhibitory M currents (K+ conductance) and provides these animals with a measure of resistance to seizures induced by the non-selective muscarinic agonist pilocarpine. AKAP5 null mice secrete less insulin from &beta;-cells, yet display improved glucose handling because of increased insulin sensitivity in target tissues.

Exon 2 of the mouse Akap5 gene was excised to create a null allele. Homozygotes have impaired motor coordination and strength, harbor deficits in spatial memory retention, and show reduced anxiety. They also secrete less insulin from &beta;-cells, yet display improved glucose handling because of increased insulin sensitivity in target tissues.

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