ArticleThe Journal of physiology1998
Role of domain I of neuronal Ca2+ channel alpha1 subunits in G protein modulation.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 38 citations in OpenAlex.
- Development of cannabidiol as a treatment for severe childhood epilepsies.British journal of pharmacology · 2020Review
- Differential Cav2.1 and Cav2.3 channel inhibition by baclofen and α-conotoxin Vc1.1 via GABAB receptor activation.The Journal of general physiology · 2014Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Inhibition of synaptic transmission and G protein modulation by synthetic CaV2.2 Ca²+ channel peptides.The Journal of physiology · 2011Article
- Attenuation of G protein-mediated inhibition of N-type calcium currents by expression of caveolins in mammalian NG108-15 cells.The Journal of physiology · 2001Article
- The C terminus of the Ca channel alpha1B subunit mediates selective inhibition by G-protein-coupled receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Identification of residues in the N terminus of alpha1B critical for inhibition of the voltage-dependent calcium channel by Gbeta gamma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Identification of the amino terminus of neuronal Ca2+ channel alpha1 subunits alpha1B and alpha1E as an essential determinant of G-protein modulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- G protein modulation of CaV2 voltage-gated calcium channels.Channels (Austin, Tex.)Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
1. We studied the G protein inhibition of heteromultimeric neuronal Ca2+ channels by constructing a series of chimeric channels between the strongly modulated alpha1B subunit and the alpha1E(rbEII) subunit, which showed no modulation. 2. In parallel studies, alpha1 subunit constructs were co-expressed together with the accessory Ca2+ channel alpha2-delta and beta2a subunits in mammalian (COS-7) cells and Xenopus oocytes. G protein inhibition of expressed Ca2+ channel currents was induced by co-transfection of Gbeta1 and Ggamma2 subunits in COS-7 cells or activation of co-expressed dopamine (D2) receptors by quinpirole (100 nM) in oocytes. 3. The data indicate that transfer of the alpha1B region containing the N-terminal, domain I and the I-II loop (i.e. the alpha1B1-483 sequence), conferred G protein modulation on alpha1E(rbEII), both in terms of a slowing of activation kinetics and a reduction in current amplitude. 4. In contrast, the data are not consistent with the I-II loop and/or the C-terminal forming a unique site for G protein modulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.