8.A.92.  The G-Protein αβγ Complex (GPC) Family 

G-proteins, including either the α-subunit (Galpha) or the βγ-subunit complex (Gbetagamma), regulate a variety of channels (TC class 1) and transport systems (carriers and primary active transporters ;TC classes 2 and 3, respectively). For example, ACh enhances calcium channel, Cav1.2b currents via muscarinic M2 receptors that couple sequentially to Gbetagamma, PI3K, a novel PKC, and c-Src (Callaghan et al. 2004), and the calcium channel, Ca_v2 is regulated by G-proteins (Currie 2010; Zamponi and Currie 2013). Also, The G protein-coupled inwardly rectifying K⁺ channel, GIRK1/GIRK4, can be activated by receptors coupled to the Galpha(i) subunit (Hill and Peralta 2001). Moreover, neuronal G protein-coupled inwardly-rectifying potassium channels (GIRKs, Kir3.x) can be activated or inhibited by distinct classes of receptors (Galphai/o and Galphaq/11-coupled, respectively), providing dynamic regulation of neuronal excitability. Lei et al. 2003 used a mammalian heterologous expression system to address mechanisms of GIRK channel regulation by Galpha and Gbetagamma subunits. Like beta1- and beta2-containing Gbetagamma dimers, GIRK channels are also activated by G protein betagamma dimers containing beta3 and beta4 subunits, but are inhibited by beta5-containing Gbetagamma dimers and/or by Galpha proteins of the Galphaq/11 family. The properties of Gbeta5-mediated inhibition suggest that beta5-containing Gbetagamma dimers act as competitive antagonists of other activating Gbetagamma pairs on GIRK channels (Lei et al. 2003). G-protein-coupled receptors control Ca²⁺ entry and Ca²⁺-dependent events such as neurotransmitter and hormone release (McDavid and Currie 2006). Finally, Gαi2 activates the TRPC4 channel by direct binding, which then induces Ca²⁺ entry (Myeong et al. 2015), and the G protein betagamma subunit complex modulates ionotropic glycine receptors, GlyRs (Yevenes et al. 2006).

Beta3 regulates the formation of transport carriers at the trans golgi nextwork (TGN), and fission of transport carriers at the TGN is dependent on PLCbeta3, which is necessary to activate PKCeta and PKD in that Golgi compartment, via DAG production (Díaz Añel 2007). 

Two Gbetagamma dimers of the Arabidopsis thaliana heterotrimeric G protein complex are differentially localized to the central and cortical tissues of the Arabidopsis roots. A null mutation in either the single beta (AGB1) or the two gamma (AGG1 and AGG2) subunits alters auxin transport (Zamponi and Currie 2013). Also, The G protein-coupled inwardly rectifying K⁺ channel, GIRK1/GIRK4, can be activated by receptors coupled to the Galpha(i) subunit (Hill and Peralta 2001). Moreover, neuronal G protein-coupled inwardly-rectifying potassium channels (GIRKs, Kir3.x) can be activated or inhibited by distinct classes of receptors (Galphai/o and Galphaq/11-coupled, respectively), providing dynamic regulation of neuronal excitability. Lei et al. 2003 used a mammalian heterologous expression system to address mechanisms of GIRK channel regulation by Galpha and Gbetagamma subunits. Like beta1- and beta2-containing Gbetagamma dimers, GIRK channels are also activated by G protein betagamma dimers containing beta3 and beta4 subunits, but are inhibited by beta5-containing Gbetagamma dimers and/or by Galpha proteins of the Galphaq/11 family. The properties of Gbeta5-mediated inhibition suggest that beta5-containing Gbetagamma dimers act as competitive antagonists of other activating Gbetagamma pairs on GIRK channels (Lei et al. 2003). G-protein-coupled receptors control Ca²⁺ entry and Ca²⁺-dependent events such as neurotransmitter and hormone release (McDavid and Currie 2006). Finally, Gαi2 activates the TRPC4 channel by direct binding, which then induces Ca²⁺ entry (Myeong et al. 2015), and the G protein betagamma subunit complex modulates ionotropic glycine receptors, GlyRs (Yevenes et al. 2006).

Beta3 regulates the formation of transport carriers at the trans golgi nextwork (TGN), and fission of transport carriers at the TGN is dependent on PLCbeta3, which is necessary to activate PKCeta and PKD in that Golgi compartment, via DAG production (Díaz Añel 2007). 

Two Gbetagamma dimers of the Arabidopsis thaliana heterotrimeric G protein complex are differentially localized to the central and cortical tissues of the Arabidopsis roots. A null mutation in either the single beta (AGB1) or the two gamma (AGG1 and AGG2) subunits alters auxin transport (Mudgil et al. 2009).