ArticleBiophysical journal2000
Calcium channel beta subunit promotes voltage-dependent modulation of alpha 1 B by G beta gamma.
Article in Biophysical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 96 citations in OpenAlex.
- Exploring the potential for gene therapy in Cav1.4-related retinal channelopathies.Channels (Austin, Tex.) · 2025Review
- Regulation of N-type calcium channels by nociceptin receptors and its possible role in neurological disorders.Molecular brain · 2022Review
- Inhibitory effects on L- and N-type calcium channels by a novel CaNaunyn-Schmiedeberg's archives of pharmacology · 2022Article
- More than a pore: How voltage-gated calcium channels act on different levels of neuronal communication regulation.Channels (Austin, Tex.) · 2021Review
- Addressing opioid tolerance and opioid-induced hypersensitivity: Recent developments and future therapeutic strategies.Pharmacology research & perspectives · 2021Review
- How Postdoctoral Research in Paul Greengard's Laboratory Shaped My Scientific Career, Although I Never Did Another Phosphorylation Assay.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Functions of Presynaptic Voltage-gated Calcium Channels.Function (Oxford, England) · 2021Review
- Presynaptic calcium channels: specialized control of synaptic neurotransmitter release.Nature reviews. Neuroscience · 2020Review
- Illuminating and Sniffing Out the Neuromodulatory Roles of Dopamine in the Retina and Olfactory Bulb.Frontiers in cellular neuroscience · 2020Review
- Calcium absorption in the fluted giant clam, Tridacna squamosa, may involve a homolog of voltage-gated calcium channel subunit α1 (CACNA1) that has an apical localization and displays light-enhanced protein expression in the ctenidium.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2019Article
- Voltage-gated calcium channels: their discovery, function and importance as drug targets.Brain and neuroscience advances · 2018Article
- Calmodulin modulates the CaIBRO reports · 2017Article
- Voltage-gated calcium channels and their auxiliary subunits: physiology and pathophysiology and pharmacology.The Journal of physiology · 2016Review
- The CaVβ Subunit Protects the I-II Loop of the Voltage-gated Calcium Channel CaV2.2 from Proteasomal Degradation but Not Oligoubiquitination.The Journal of biological chemistry · 2016Article
- Genetic disruption of voltage-gated calcium channels in psychiatric and neurological disorders.Progress in neurobiology · 2015Review
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- 14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.The Journal of biological chemistry · 2015Article
- The Gβγ-Src signaling pathway regulates TNF-induced necroptosis via control of necrosome translocation.Cell research · 2014Article
- 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
- Modal gating of GluN1/GluN2D NMDA receptors.Neuropharmacology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-dependent calcium channels (VDCCs) are heteromultimers composed of a pore-forming alpha1 subunit and auxiliary subunits, including the intracellular beta subunit, which has a strong influence on the channel properties. Voltage-dependent inhibitory modulation of neuronal VDCCs occurs primarily by activation of G-proteins and elevation of the free G beta gamma dimer concentration. Here we have examined the interaction between the regulation of N-type (alpha 1 B) channels by their beta subunits and by G beta gamma dimers, heterologously expressed in COS-7 cells. In contrast to previous studies suggesting antagonism of G protein inhibition by the VDCC beta subunit, we found a significantly larger G beta gamma-dependent inhibition of alpha 1 B channel activation when the VDCC alpha 1 B and beta subunits were coexpressed. In the absence of coexpressed VDCC beta subunit, the G beta gamma dimers, either expressed tonically or elevated via receptor activation, did not produce the expected features of voltage-dependent G protein modulation of N-type channels, including slowed activation and prepulse facilitation, while VDCC beta subunit coexpression restored all of the hallmarks of G beta gamma modulation. These results suggest that the VDCC beta subunit must be present for G beta gamma to induce voltage-dependent modulation of N-type calcium channels.
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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.