Evidence map›Paper›PMID 1314395›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1992

The synaptic vesicle protein synaptotagmin associates with calcium channels and is a putative Lambert-Eaton myasthenic syndrome antigen.

C Leveque, T Hoshino, P David, Y Shoji-Kasai, K Leys, A Omori, B Lang, O el Far, K Sato, N Martin-Moutot

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
12.8field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 219 citations in OpenAlex.

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  15. Dual roles of the C2B domain of synaptotagmin I in synchronizing Ca2+-dependent neurotransmitter release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  16. Review
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  18. Targeted mutations in the syntaxin H3 domain specifically disrupt SNARE complex function in synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  19. Rapid regulated dense-core vesicle exocytosis requires the CAPS protein.Proceedings of the National Academy of Sciences of the United States of America · 2000
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  20. Article
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

10 authors at 1 institution in 1 country.

C LevequeNeurobiologie des Canaux Ioniques, Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Secteur Nord, Marseille, France.
T Hoshino
P David
Y Shoji-Kasai
K Leys
A Omori
B Lang
O el Far
K Sato
N Martin-Moutot
Institut de Neurobiologie de la Méditerranée · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin G fractions from patients with Lambert-Eaton myasthenic syndrome (LEMS), an autoimmune disease of neuromuscular transmission, immunoprecipitate 125I-labeled omega-conotoxin GVIA-labeled calcium channels solubilized from rat brain. A 58-kDa antigen was detected by probing Western blots of partially purified calcium channels with LEMS plasma and IgG and was shown to be the relevant antigen in omega-conotoxin receptor immunoprecipitation. Monoclonal antibody 1D12, produced by immunizing mice with synaptic membranes, has properties similar to these autoimmune IgGs in both immunoprecipitation and Western blotting assays. 1D12 antigen was purified by immunoaffinity chromatography and shown to bind LEMS IgG. The antigen was identified by screening a rat brain cDNA library with 1D12 and was found to have strong homology to the synaptic vesicle membrane protein synaptotagmin. Our results indicate therefore that these antibodies immunoprecipitate omega-conotoxin receptors by binding to synaptotagmin that is associated with calcium channels. We suggest that the interaction between synaptotagmin and the voltage-gated calcium channel plays a role in docking synaptic vesicles at the plasma membrane prior to rapid neurotransmitter release and that autoantibody binding to a synaptotagmin-calcium-channel complex may be involved in the etiology of LEMS.

Indexed as

Calcium-Binding ProteinsAntibodies, MonoclonalAntigensBlotting, WesternCalcium ChannelsHumansImmunoglobulin GLambert-Eaton Myasthenic SyndromeMembrane GlycoproteinsMollusk VenomsNerve Tissue Proteinsomega-Conotoxin GVIAPeptides, CyclicReceptors, NeurotransmitterSynaptic VesiclesSynaptotagminsAntibodies, MonoclonalAntigensCalcium-Binding ProteinsCalcium ChannelsImmunoglobulin GMembrane GlycoproteinsMollusk VenomsNerve Tissue Proteinsomega-Conotoxin GVIAomega-conotoxin receptorPeptides, CyclicReceptors, NeurotransmitterSynaptotagmins

Identifiers

PMID1314395
PMCPMC48921
OpenAlexW2066953895

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.