Evidence map›Paper›PMID 24133283›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

The neural cell adhesion molecule promotes maturation of the presynaptic endocytotic machinery by switching synaptic vesicle recycling from adaptor protein 3 (AP-3)- to AP-2-dependent mechanisms.

Aparna Shetty, Vladimir Sytnyk, Iryna Leshchyns'ka, Dmytro Puchkov, Volker Haucke, Melitta Schachner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

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  12. A genetically defined disease model reveals that urothelial cells can initiate divergent bladder cancer phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Article
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  15. Postnatal Restriction of Activity-Induced CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  16. Article
  17. Retromer in Synaptic Function and Pathology.Frontiers in synaptic neuroscience · 2018
    Review
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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

6 authors at 4 institutions in 4 countries.

Aparna ShettyZentrum für Molekulare Neurobiologie, Universität Hamburg, 20246 Hamburg, Germany, School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, New South Wales 2052, Australia, Leibniz Institut für Molekulare Pharmakologie and Freie Universität Berlin, 13125 Berlin, Germany, Keck Center for Collaborative Neuroscience, Rutgers University, Piscataway, New Jersey 08854-8082, and Center for Neuroscience, Shantou University Medical College, Shantou 515041, People's Republic of China.
Vladimir Sytnyk
Iryna Leshchyns'ka
Dmytro Puchkov
Volker Haucke
Melitta Schachner
Universität Hamburg · DELeibniz-Forschungsinstitut für Molekulare Pharmakologie · DERutgers, The State University of New Jersey · USUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Newly formed synapses undergo maturation during ontogenetic development via mechanisms that remain poorly understood. We show that maturation of the presynaptic endocytotic machinery in CNS neurons requires substitution of the adaptor protein 3 (AP-3) with AP-2 at the presynaptic plasma membrane. In mature synapses, AP-2 associates with the intracellular domain of the neural cell adhesion molecule (NCAM). NCAM promotes binding of AP-2 over binding of AP-3 to presynaptic membranes, thus favoring the substitution of AP-3 for AP-2 during formation of mature synapses. The presynaptic endocytotic machinery remains immature in adult NCAM-deficient (NCAM-/-) mice accumulating AP-3 instead of AP-2 and its partner protein AP180 in synaptic membranes and vesicles. NCAM deficiency or disruption of the NCAM/AP-2 complex in wild-type (NCAM+/+) neurons by overexpression of AP-2 binding-defective mutant NCAM interferes with efficient retrieval of the synaptic vesicle v-SNARE synaptobrevin 2. Abnormalities in synaptic vesicle endocytosis and recycling may thus contribute to neurological disorders associated with mutations in NCAM.

Indexed as

Adaptor Protein Complex 2Adaptor Protein Complex 3AnimalsCHO CellsCricetulusEndocytosisHEK293 CellsHippocampusHumansMiceMice, KnockoutNeural Cell Adhesion MoleculesNeuronsPresynaptic TerminalsSynaptic MembranesSynaptic VesiclesAdaptor Protein Complex 2Adaptor Protein Complex 3Neural Cell Adhesion MoleculesVesicle-Associated Membrane Protein 2

Identifiers

PMID24133283
PMCPMC6618524
OpenAlexW1971126467

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.