RT Journal Article SR Electronic T1 Ca2+ Channels As Integrators of G Protein-Mediated Signaling in Neurons JF Molecular Pharmacology JO Mol Pharmacol FD American Society for Pharmacology and Experimental Therapeutics SP 1071 OP 1076 DO 10.1124/mol.104.002261 VO 66 IS 5 A1 Strock, Jesse A1 Diversé-Pierluissi, María A. YR 2004 UL http://molpharm.aspetjournals.org/content/66/5/1071.abstract AB The observations from Dunlap and Fischbach that transmitter-mediated shortening of the duration of action potentials could be caused by a decrease in calcium conductance led to numerous studies of the mechanisms of modulation of voltage-dependent calcium channels. Calcium channels are well known targets for inhibition by receptor-G protein pathways, and multiple forms of inhibition have been described. Inhibition of Ca2+ channels can be mediated by G protein βγ-subunits or by kinases, such as protein kinase C and tyrosine kinases. In the last few years, it has been shown that integration of G protein signaling can take place at the level of the calcium channel by regulation of the interaction of the channel pore-forming subunit with different cellular proteins.