Evidence map›Paper›PMID 9634547›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

Identification of the amino terminus of neuronal Ca2+ channel alpha1 subunits alpha1B and alpha1E as an essential determinant of G-protein modulation.

K M Page, C Cantí, G J Stephens, N S Berrow, A C Dolphin

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 123 citations in OpenAlex.

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  11. Article
  12. The Role of Calcium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016
    Review
  13. Alternative Splicing in Ca(V)2.2 Regulates Neuronal Trafficking via Adaptor Protein Complex-1 Adaptor Protein Motifs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  14. Article
  15. Article
  16. Review
  17. Article
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  19. Article
  20. Voltage-gated calcium channels.Cold Spring Harbor perspectives in biology · 2011
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

K M PageDepartment of Pharmacology, University College London, London WC1E 6BT, United Kingdom.
C Cantí
G J Stephens
N S Berrow
A C Dolphin
University College London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

We have examined the basis for G-protein modulation of the neuronal voltage-dependent calcium channels (VDCCs) alpha1E and alpha1B. A novel PCR product of alpha1E was isolated from rat brain. This contained an extended 5' DNA sequence and was subcloned onto the previously cloned isoform rbEII, giving rise to alpha1Elong whose N terminus was extended by 50 amino acids. VDCC alpha1 subunit constructs were co-expressed with the accessory alpha2-delta and beta2a subunits in Xenopus oocytes and mammalian (COS-7) cells. The alpha1Elong showed biophysical properties similar to those of rbEII; however, when G-protein modulation of expressed alpha1 subunits was induced by activation of co-expressed dopamine (D2) receptors with quinpirole (100 nM) in oocytes, or by co-transfection of Gbeta1gamma2 subunits in COS-7 cells, alpha1Elong, unlike alpha1E(rbEII), was found to be G-protein-modulated, in terms of both a slowing of activation kinetics and a reduction in current amplitude. However, alpha1Elong showed less modulation than alpha1B, and substitution of the alpha1E1-50 with the corresponding region of alpha1B1-55 produced a chimera alpha1bEEEE, with G-protein modulation intermediate between alpha1Elong and alpha1B. Furthermore, deletion of the N-terminal 1-55 sequence from alpha1B produced alpha1BDeltaN1-55, which could not be modulated, thus identifying the N-terminal domain as essential for G-protein modulation. Taken together with previous studies, these results indicate that the intracellular N terminus of alpha1E1-50 and alpha1B1-55 is likely to contribute to a multicomponent site, together with the intracellular I-II loop and/or the C-terminal tail, which are involved in Gbetagamma binding and/or in subsequent modulation of channel gating.

Indexed as

Calcium Channels, N-TypeAnimalsBrain ChemistryCalcium ChannelsCalcium Channels, R-TypeCation Transport ProteinsCattleCOS CellsDopamine AgonistsGene ExpressionGTP-Binding ProteinsGuanosine DiphosphateIon Channel GatingIsomerismKineticsMolecular Sequence DataCacna1e protein, ratCalcium ChannelsCalcium Channels, N-TypeCalcium Channels, R-TypeCation Transport ProteinsDopamine AgonistsGTP-Binding Proteinsguanosine 5'-O-(2-thiodiphosphate)Guanosine DiphosphateNerve Tissue ProteinsQuinpiroleThionucleotides

Identifiers

PMID9634547
PMCPMC6792552
OpenAlexW2113130197

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.