ReviewBiochimica et biophysica acta2013
Regulation of Ca(V)2 calcium channels by G protein coupled receptors.
Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 206 citations in OpenAlex.
- The C825T Polymorphism of the G-Protein β3 Gene as a Risk Factor for Depression: A Meta-Analysis.PloS one · 2015Pooled it
- Magnesium Attenuates the Association Between Mixed Element Exposure and Depressive Symptoms in Older Adults.Toxics · 2026Article
- Nociceptor-enriched CAPS1 isoform couples to CabioRxiv : the preprint server for biology · 2026Article
- Depression of synaptic outputs by reduction of CaFrontiers in molecular neuroscience · 2026Article
- Age-Dependent Regulation of Acetylcholine Release at the Neuromuscular Junction Mediated by GABA.Cells · 2025Article
- Developmental regulation of GABAHistology and histopathology · 2025Article
- GαScience signaling · 2025Article
- Neuromodulation of voltage-gated sodium channels by Gβ1γ2 subunits: Implications for GNB1-linked encephalopathy.Neurobiology of disease · 2025Article
- A rich conformational palette underlies human CaNature communications · 2025Article
- Nanoarchitecture of CaBrain pathology (Zurich, Switzerland) · 2025Article
- In vitro human ion channel assays predictive of drug-induced seizure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- A concise mathematical description of signal transformations across the hippocampal apical CA3 to CA1 dendritic response.Frontiers in neural circuits · 2025Article
- Voltage-dependent G-protein regulation of CaScience advances · 2024Article
- Peptide and Peptidomimetic Inhibitors Targeting the Interaction of Collapsin Response Mediator Protein 2 with the N-Type Calcium Channel for Pain Relief.ACS pharmacology & translational science · 2024Review
- Article
- The Mechanism of α2 adrenoreceptor-dependent Modulation of Neurotransmitter Release at the Neuromuscular Junctions.Neurochemical research · 2024Article
- Serotonin and the serotonin transporter in the adrenal gland.Vitamins and hormones · 2024Review
- Active Zone Trafficking of CaV2/UNC-2 Channels Is Independent of β/CCB-1 and α2δ/UNC-36 Subunits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Physiologic and Nanoscale Distinctions Define Glutamatergic Synapses in Tonic vs Phasic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Histaminergic regulation of food intake.Frontiers in endocrinology · 2023Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Voltage gated calcium channels (Ca²⁺ channels) are key mediators of depolarization induced calcium influx into excitable cells, and thereby play pivotal roles in a wide array of physiological responses. This review focuses on the inhibition of Ca(V)2 (N- and P/Q-type) Ca²⁺-channels by G protein coupled receptors (GPCRs), which exerts important autocrine/paracrine control over synaptic transmission and neuroendocrine secretion. Voltage-dependent inhibition is the most widespread mechanism, and involves direct binding of the G protein βγ dimer (Gβγ) to the α1 subunit of Ca(V)2 channels. GPCRs can also recruit several other distinct mechanisms including phosphorylation, lipid signaling pathways, and channel trafficking that result in voltage-independent inhibition. Current knowledge of Gβγ-mediated inhibition is reviewed, including the molecular interactions involved, determinants of voltage-dependence, and crosstalk with other cell signaling pathways. A summary of recent developments in understanding the voltage-independent mechanisms prominent in sympathetic and sensory neurons is also included. This article is part of a Special Issue entitled: Calcium channels.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.