Evidence map›Paper›PMID 20610389›Full record

ArticleThe Journal of biological chemistry2010

Functional consequences of the interactions among the neural cell adhesion molecule NCAM, the receptor tyrosine kinase TrkB, and the inwardly rectifying K+ channel KIR3.3.

Ralf Kleene, Claas Cassens, Robert Bähring, Thomas Theis, Mei-Fang Xiao, Alexander Dityatev, Claus Schafer-Nielsen, Frank Döring, Erhard Wischmeyer, Melitta Schachner

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Effects ofEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  6. Article
  7. GIRK3 gates activation of the mesolimbic dopaminergic pathway by ethanol.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  8. Mice with compromised 5-HTT function lack phosphotyrosine-mediated inhibitory control over prefrontal 5-HT responses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  9. Neural cell adhesion molecule-mediated Fyn activation promotes GABAergic synapse maturation in postnatal mouse cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  10. Article
  11. 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

10 authors at 5 institutions in 3 countries.

Ralf KleeneZentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 85, 20246 Hamburg, Germany.
Claas Cassens
Robert Bähring
Thomas Theis
Mei-Fang Xiao
Alexander Dityatev
Claus Schafer-Nielsen
Frank Döring
Erhard Wischmeyer
Melitta Schachner
Martini-Klinik · DEUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity of Würzburg · DESchafer-N (Denmark) · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell adhesion molecules and neurotrophin receptors are crucial for the development and the function of the nervous system. Among downstream effectors of neurotrophin receptors and recognition molecules are ion channels. Here, we provide evidence that G protein-coupled inwardly rectifying K(+) channel Kir3.3 directly binds to the neural cell adhesion molecule (NCAM) and neurotrophin receptor TrkB. We identified the binding sites for NCAM and TrkB at the C-terminal intracellular domain of Kir3.3. The interaction between NCAM, TrkB, and Kir3.3 was supported by immunocytochemical co-localization of Kir3.3, NCAM, and/or TrkB at the surface of hippocampal neurons. Co-expression of TrkB and Kir3.1/3.3 in Xenopus oocytes increased the K(+) currents evoked by Kir3.1/3.3 channels. This current enhancement was reduced by the concomitant co-expression with NCAM. Both surface fluorescence measurements of microinjected oocytes and cell surface biotinylation of transfected CHO cells indicated that the cell membrane localization of Kir3.3 is regulated by TrkB and NCAM. Furthermore, the level of Kir3.3, but not of Kir3.2, at the plasma membranes was reduced in TrkB-deficient mice, supporting the notion that TrkB regulates the cell surface expression of Kir3.3. The premature expression of developmentally late appearing Kir3.1/3.3 in hippocampal neurons led to a reduction of NCAM-induced neurite outgrowth. Our observations indicate a decisive role for the neuronal K(+) channel in regulating NCAM-dependent neurite outgrowth and attribute a physiologically meaningful role to the functional interplay of Kir3.3, NCAM, and TrkB in ontogeny.

Indexed as

AnimalsCell AdhesionCell MembraneCHO CellsCricetinaeCricetulusGene Expression RegulationG Protein-Coupled Inwardly-Rectifying Potassium ChannelsHippocampusHumansMiceMice, KnockoutNeural Cell Adhesion MoleculesNeuritesOocytesProtein BindingG Protein-Coupled Inwardly-Rectifying Potassium ChannelsKCNJ6 protein, humanKcnj6 protein, mouseNeural Cell Adhesion MoleculesReceptor, trkB

Identifiers

PMID20610389
PMCPMC2937924
OpenAlexW2092838804

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.