Expression of the CaM mutant also prevented receptor-mediated ERK1,2 phosphorylation in cultured cortical neurons and choroid plexus epithelial cells that endogenously express 5-HT (2C) receptors.
These findings demonstrate that physical interaction of CaM with recombinant and native 5-HT (2C) receptors is critical for G protein-independent, arrestin-dependent receptor signaling.