ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Identification of residues in the N terminus of alpha1B critical for inhibition of the voltage-dependent calcium channel by Gbeta gamma.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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
52 citing papers in PubMed, 124 citations in OpenAlex.
- Voltage-dependent G-protein regulation of CaScience advances · 2024Article
- Epilepsy-linked kinase CDKL5 phosphorylates voltage-gated calcium channel Cav2.3, altering inactivation kinetics and neuronal excitability.Nature communications · 2023Article
- Inactivation influences the extent of inhibition of voltage-gated CaFrontiers in physiology · 2023Article
- 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
- Modulation of voltage-gated CaChannels (Austin, Tex.) · 2020Review
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- GPCR regulation of secretion.Pharmacology & therapeutics · 2018Review
- Alternative Splicing at N Terminus and Domain I Modulates CaBiophysical journal · 2018Article
- New Insights Into Interactions of Presynaptic Calcium Channel Subtypes and SNARE Proteins in Neurotransmitter Release.Frontiers in molecular neuroscience · 2018Article
- Voltage-gated calcium channels and their auxiliary subunits: physiology and pathophysiology and pharmacology.The Journal of physiology · 2016Review
- A CaV2.1 N-terminal fragment relieves the dominant-negative inhibition by an Episodic ataxia 2 mutant.Neurobiology of disease · 2016Article
- The Role of Calcium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Ethanol effects on glycinergic transmission: From molecular pharmacology to behavior responses.Pharmacological research · 2015Review
- The inhibition of functional expression of calcium channels by prion protein demonstrates competition with α2δ for GPI-anchoring pathways.The Biochemical journal · 2014Article
- The amino-terminus of high voltage activated calcium channels: CaM you or can't you?Channels (Austin, Tex.) · 2014Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- GPCR mediated regulation of synaptic transmission.Progress in neurobiology · 2012Review
- The basic property of Lys385 is important for potentiation of the human α1 glycine receptor by ethanol.The Journal of pharmacology and experimental therapeutics · 2012Article
- Voltage-gated calcium channels.Cold Spring Harbor perspectives in biology · 2011Review
- Inhibition of synaptic transmission and G protein modulation by synthetic CaV2.2 Ca²+ channel peptides.The Journal of physiology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
To examine the role of the intracellular N terminus in the G-protein modulation of the neuronal voltage-dependent calcium channel (VDCC) alpha1B, we have pursued two routes of investigation. First, we made chimeric channels between alpha1B and alpha1C, the latter not being modulated by Gbeta gamma subunits. VDCC alpha1 subunit constructs were coexpressed with accessory alpha2delta and beta2a subunits in Xenopus oocytes and mammalian (COS-7) cells. G-protein modulation of expressed alpha1 subunits was induced by activation of coexpressed dopamine (D2) receptors with quinpirole in oocytes, or by cotransfection of Gbeta1gamma2 subunits in COS-7 cells. For the chimeric channels, only those with the N terminus of alpha1B showed any G-protein modulation; further addition of the first transmembrane domain and I-II intracellular linker of alpha1B increased the degree of modulation. To determine the amino acids within the alpha1B N terminus, essential for G-protein modulation, we made mutations of this sequence and identified three amino acids (S48, R52, and R54) within an 11 amino acid sequence as being critical for G-protein modulation, with I49 being involved to a lesser extent. This sequence may comprise an essential part of a complex Gbeta gamma-binding site or be involved in its subsequent action.
Indexed as
Identifiers
10436043PMC6782846W2163071159What 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.