ArticleProceedings of the National Academy of Sciences of the United States of America2001
Allosteric modulation of Ca2+ channels by G proteins, voltage-dependent facilitation, protein kinase C, and Ca(v)beta subunits.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 69 citations in OpenAlex.
- PKC in the perspective of dopamine receptor signaling.Acta biochimica Polonica · 2025Review
- Retinoid receptor-based signaling plays a role in voltage-dependent inhibition of invertebrate voltage-gated CaThe Journal of biological chemistry · 2019Article
- Protein kinase C activity is a protective modifier of Purkinje neuron degeneration in cerebellar ataxia.Human molecular genetics · 2018Article
- Long-range coupling between the extracellular gates and the intracellular ATP binding domains of multidrug resistance protein pumps and cystic fibrosis transmembrane conductance regulator channels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Article
- An electrostatic interaction at the tetrahelix bundle promotes phosphorylation-dependent cystic fibrosis transmembrane conductance regulator (CFTR) channel opening.The Journal of biological chemistry · 2014Article
- Protein kinase C activation decreases peripheral actin network density and increases central nonmuscle myosin II contractility in neuronal growth cones.Molecular biology of the cell · 2013Article
- GABAB receptor-mediated frequency-dependent and circadian changes in synaptic plasticity modulate retinal input to the suprachiasmatic nucleus.The Journal of physiology · 2013Article
- Activation of alpha1-adrenoceptors enhances glutamate release onto ventral tegmental area dopamine cells.Neuroscience · 2012Article
- Inhibition of synaptic transmission and G protein modulation by synthetic CaV2.2 Ca²+ channel peptides.The Journal of physiology · 2011Article
- Calcium-dependent phosphorylation regulates neuronal stability and plasticity in a highly precise pacemaker nucleus.Journal of neurophysiology · 2011Article
- Differential modulation of N-type calcium channels by micro-opioid receptors in oxytocinergic versus vasopressinergic neurohypophysial terminals.Journal of cellular physiology · 2010Article
- Interactions between the amyloid precursor protein C-terminal domain and G proteins mediate calcium dysregulation and amyloid beta toxicity in Alzheimer's disease.The FEBS journal · 2009Article
- Facilitation versus depression in cultured hippocampal neurons determined by targeting of Ca2+ channel Cavbeta4 versus Cavbeta2 subunits to synaptic terminals.The Journal of cell biology · 2007Article
- RGS9-2 modulates D2 dopamine receptor-mediated Ca2+ channel inhibition in rat striatal cholinergic interneurons.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Cavbeta-subunit displacement is a key step to induce the reluctant state of P/Q calcium channels by direct G protein regulation.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Intracellular Na+ inhibits voltage-dependent N-type Ca2+ channels by a G protein betagamma subunit-dependent mechanism.The Journal of physiology · 2004Article
- Beta subunits of voltage-gated calcium channels.Journal of bioenergetics and biomembranes · 2003Review
- Neurosteroids shift partial agonist activation of GABA(A) receptor channels from low- to high-efficacy gating patterns.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- The familial hemiplegic migraine mutation R192Q reduces G-protein-mediated inhibition of P/Q-type (Ca(V)2.1) calcium channels expressed in human embryonic kidney cells.The Journal of physiology · 2003Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
N-type and P/Q-type Ca(2+) channels are inhibited by neurotransmitters acting through G protein-coupled receptors in a membrane-delimited pathway involving Gbetagamma subunits. Inhibition is caused by a shift from an easily activated "willing" (W) state to a more-difficult-to-activate "reluctant" (R) state. This inhibition can be reversed by strong depolarization, resulting in prepulse facilitation, or by protein kinase C (PKC) phosphorylation. Comparison of regulation of N-type Ca(2+) channels containing Cav2.2a alpha(1) subunits and P/Q-type Ca(2+) channels containing Ca(v)2.1 alpha(1) subunits revealed substantial differences. In the absence of G protein modulation, Ca(v)2.1 channels containing Ca(v)beta subunits were tonically in the W state, whereas Ca(v)2.1 channels without beta subunits and Ca(v)2.2a channels with beta subunits were tonically in the R state. Both Ca(v)2.1 and Ca(v)2.2a channels could be shifted back toward the W state by strong depolarization or PKC phosphorylation. Our results show that the R state and its modulation by prepulse facilitation, PKC phosphorylation, and Ca(v)beta subunits are intrinsic properties of the Ca(2+) channel itself in the absence of G protein modulation. A common allosteric model of G protein modulation of Ca(2+)-channel activity incorporating an intrinsic equilibrium between the W and R states of the alpha(1) subunits and modulation of that equilibrium by G proteins, Ca(v)beta subunits, membrane depolarization, and phosphorylation by PKC accommodates our findings. Such regulation will modulate transmission at synapses that use N-type and P/Q-type Ca(2+) channels to initiate neurotransmitter release.
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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.