properties due to palmitoylation and RNA editing. Other forms of modulation on the β subunit include increasing or decreasing of the subunit's expression. This is due to the fact that β subunits increase the open-probability of the channel, activity in the plasma membrane, and antagonize the ubiquitination of the channel. L-type calcium channels are also modulated by G protein-coupled receptors and the adrenergic nervous system. Protein Kinase A (PKA) activated by a G protein-coupled receptors cascade can phosphorylate L-type calcium channels, after channels form a signaling complex with A-Kinase-Anchoring proteins (AKAPs) , to increase calcium current through the channel, increasing the open-state probability, and an accelerated recovery period. Activated Phospholipase C (PLC) from G protein-coupled receptors can breakdown polyphosphoinositides to decrease the channels calcium current by 20%-30%. The adrenergic nervous system has been seen to modulate L-type calcium channels by cleaving the C-terminal fragment when the β-adrenergic receptor is stimulated to increase activation of the channels. Genes , , , See also CACNA1C CACNA1D CACNA1S CACNA1F References Further reading External links Ion channels Electrophysiology Membrane biology Integral membrane proteins Calcium channels