ArticlePflugers Archiv : European journal of physiology2009
Determinants of the voltage dependence of G protein modulation within calcium channel beta subunits.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023Article
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- Increase of CaBMC research notes · 2018Article
- Phosphorylation sites in the Hook domain of CaVβ subunits differentially modulate CaV1.2 channel function.Journal of molecular and cellular cardiology · 2015Article
- Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Structure and function of the β subunit of voltage-gated Ca²⁺ channels.Biochimica et biophysica acta · 2013Review
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- A quartet of leucine residues in the guanylate kinase domain of CaVβ determines the plasma membrane density of the CaV2.3 channel.The Journal of biological chemistry · 2012Article
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- Functional dissection of the intramolecular Src homology 3-guanylate kinase domain coupling in voltage-gated Ca2+ channel beta-subunits.FEBS letters · 2009Article
- Origin of the voltage dependence of G-protein regulation of P/Q-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- G protein modulation of CaV2 voltage-gated calcium channels.Channels (Austin, Tex.)Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
CaVbeta subunits of voltage-gated calcium channels contain two conserved domains, a src-homology-3 (SH3) domain and a guanylate kinase-like (GK) domain with an intervening HOOK domain. We have shown in a previous study that, although Gbetagamma-mediated inhibitory modulation of CaV2.2 channels did not require the interaction of a CaVbeta subunit with the CaValpha1 subunit, when such interaction was prevented by a mutation in the alpha1 subunit, G protein modulation could not be removed by a large depolarization and showed voltage-independent properties (Leroy et al., J Neurosci 25:6984-6996, 2005). In this study, we have investigated the ability of mutant and truncated CaVbeta subunits to support voltage-dependent G protein modulation in order to determine the minimal domain of the CaVbeta subunit that is required for this process. We have coexpressed the CaVbeta subunit constructs with CaV2.2 and alpha2delta-2, studied modulation by the activation of the dopamine D2 receptor, and also examined basal tonic modulation. Our main finding is that the CaVbeta subunit GK domains, from either beta1b or beta2, are sufficient to restore voltage dependence to G protein modulation. We also found that the removal of the variable HOOK region from beta2a promotes tonic voltage-dependent G protein modulation. We propose that the absence of the HOOK region enhances Gbetagamma binding affinity, leading to greater tonic modulation by basal levels of Gbetagamma. This tonic modulation requires the presence of an SH3 domain, as tonic modulation is not supported by any of the CaVbeta subunit GK domains alone.
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