Evidence map›Paper›PMID 30881339›Full record

ArticleFrontiers in neurology2019

An Assay to Determine Mechanisms of Rapid Autoantibody-Induced Neurotransmitter Receptor Endocytosis and Vesicular Trafficking in Autoimmune Encephalitis.

Elsie Amedonu, Christoph Brenker, Sumanta Barman, Julian A Schreiber, Sebastian Becker, Stefan Peischard, Nathalie Strutz-Seebohm, Christine Strippel, Andre Dik, Hans-Peter Hartung and 8 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

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

18 authors at 3 institutions in 1 country.

Elsie AmedonuMyocellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases, University of Muenster, Muenster, Germany.
Christoph BrenkerCentre of Reproductive Medicine and Andrology, University of Muenster, Muenster, Germany.
Sumanta BarmanDepartment of Neurology, Universitätsklinikum and Center for Neurology and Neuropsychiatry LVR Klinikum, Heinrich Heine University Duesseldorf, Duesseldorf, Germany.
Julian A SchreiberMyocellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases, University of Muenster, Muenster, Germany.
Sebastian BeckerMyocellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases, University of Muenster, Muenster, Germany.
Stefan PeischardMyocellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases, University of Muenster, Muenster, Germany.
Nathalie Strutz-SeebohmMyocellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases, University of Muenster, Muenster, Germany.
Christine StrippelDepartment of Neurology, University of Muenster, Muenster, Germany.
Andre DikDepartment of Neurology, University of Muenster, Muenster, Germany.
Hans-Peter HartungDepartment of Neurology, Universitätsklinikum and Center for Neurology and Neuropsychiatry LVR Klinikum, Heinrich Heine University Duesseldorf, Duesseldorf, Germany.
Thomas BuddeInstitute for Physiology I, University of Muenster, Muenster, Germany.
Heinz WiendlDepartment of Neurology, University of Muenster, Muenster, Germany.
Timo StrünkerCentre of Reproductive Medicine and Andrology, University of Muenster, Muenster, Germany.
Bernhard WünschInstitute for Pharmaceutical and Medical Chemistry, University of Muenster, Muenster, Germany.
Norbert GoebelsDepartment of Neurology, Universitätsklinikum and Center for Neurology and Neuropsychiatry LVR Klinikum, Heinrich Heine University Duesseldorf, Duesseldorf, Germany.
Sven G MeuthDepartment of Neurology, University of Muenster, Muenster, Germany.
Guiscard SeebohmMyocellular Electrophysiology and Molecular Biology, Institute for Genetics of Heart Diseases, University of Muenster, Muenster, Germany.
Nico MelzerDepartment of Neurology, University of Muenster, Muenster, Germany.
University of Münster · DEDüsseldorf University Hospital · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-Methyl-D-aspartate (NMDA) receptors (NMDARs) are among the most important excitatory neurotransmitter receptors in the human brain. Autoantibodies to the human NMDAR cause the most frequent form of autoimmune encephalitis involving autoantibody-mediated receptor cross-linking and subsequent internalization of the antibody-receptor complex. This has been deemed to represent the predominant antibody effector mechanism depleting the NMDAR from the synaptic and extra-synaptic neuronal cell membrane. To assess in detail the molecular mechanisms of autoantibody-induced NMDAR endocytosis, vesicular trafficking, and exocytosis we transiently co-expressed rat GluN1-1a-EGFP and GluN2B-ECFP alone or together with scaffolding postsynaptic density protein 95 (PSD-95), wild-type (WT), or dominant-negative (DN) mutant Ras-related in brain (RAB) proteins (RAB5WT, RAB5DN, RAB11WT, RAB11DN) in HEK 293T cells. The cells were incubated with a pH-rhodamine-labeled human recombinant monoclonal GluN1 IgG1 autoantibody (GluN1-aAb

Indexed as

autoantibodiesautoimmune encephalitiscross-linkingendocytosisexocytosisN-Methyl-D-aspartate receptorsvesicular trafficking

Identifiers

PMID30881339
PMCPMC6405626
OpenAlexW2918533404

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.