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lüll G protein modulation of CaV2 voltage-gated calcium channels Currie KPChannels (Austin) 2010[Nov]; 4 (6): 497-509Voltage-gated Ca(2+) channels translate the electrical inputs of excitable cells into biochemical outputs by controlling influx of the ubiquitous second messenger Ca(2+) . As such the channels play pivotal roles in many cellular functions including the triggering of neurotransmitter and hormone release by CaV2.1 (P/Q-type) and CaV2.2 (N-type) channels. It is well established that G protein coupled receptors (GPCRs) orchestrate precise regulation neurotransmitter and hormone release through inhibition of CaV2 channels. Although the GPCRs recruit a number of different pathways, perhaps the most prominent, and certainly most studied among these is the so-called voltage-dependent inhibition mediated by direct binding of Gbetagamma to the alpha1 subunit of CaV2 channels. This article will review the basics of Ca(2+) -channels and G protein signaling, and the functional impact of this now classical inhibitory mechanism on channel function. It will also provide an update on more recent developments in the field, both related to functional effects and crosstalk with other signaling pathways, and advances made toward understanding the molecular interactions that underlie binding of Gbetagamma to the channel and the voltage-dependence that is a signature characteristic of this mechanism.|*Calcium Signaling[MESH]|*Ion Channel Gating[MESH]|Animals[MESH]|Calcium Channels, L-Type/metabolism[MESH]|Calcium Channels, P-Type/metabolism[MESH]|Calcium Channels, Q-Type/metabolism[MESH]|Calcium Channels/chemistry/*metabolism[MESH]|GTP-Binding Protein beta Subunits/chemistry/*metabolism[MESH]|GTP-Binding Protein gamma Subunits/chemistry/*metabolism[MESH]|Humans[MESH]|Membrane Potentials[MESH]|Models, Molecular[MESH]|Protein Conformation[MESH]|Receptors, G-Protein-Coupled/metabolism[MESH]|Structure-Activity Relationship[MESH] |