Abstract
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.
- Received May 3, 2004.
- Accepted July 19, 2004.
- The American Society for Pharmacology and Experimental Therapeutics
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In this issue
Ca2+ Channels As Integrators of G Protein-Mediated Signaling in Neurons
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- Abstract
- Classification and Structure of High-Voltage-Activated Calcium Channels
- Mechanisms of G Protein-Mediated Modulation of Cav2.2 Channels
- Integration in Loop I–II: Cross-Talk between G Protein βγ Subunits and Protein Kinase C
- Integration between GPCR and Tyrosine Kinase Signaling at the Level of the Calcium Channel
- RGS3 and Calcium-Dependence of Transmitter-Mediated Inhibition of Cav2.2 Channels
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