Evidence map›Paper›PMID 25288737›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Netrin-4 regulates thalamocortical axon branching in an activity-dependent fashion.

Yasufumi Hayano, Kensuke Sasaki, Nami Ohmura, Makoto Takemoto, Yurie Maeda, Toshihide Yamashita, Yoshio Hata, Kazuhiro Kitada, Nobuhiko Yamamoto

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  16. A network map of netrin receptor UNC5B-mediated signaling.Journal of cell communication and signaling · 2019
    Article
  17. Review
  18. Review
  19. Mutations in the netrin-1 gene cause congenital mirror movements.The Journal of clinical investigation · 2017
    Article
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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

9 authors at 3 institutions in 1 country.

Yasufumi HayanoLaboratory of Cellular and Molecular Neurobiology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan; Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan; and.
Kensuke SasakiLaboratory of Cellular and Molecular Neurobiology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan;
Nami OhmuraDivision of Integrative Bioscience, Institute of Regenerative Medicine and Biofunction, Tottori University Graduate School of Medical Sciences, 86 Nishicho, Yonago 683-8503, Japan;
Makoto TakemotoLaboratory of Cellular and Molecular Neurobiology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan;
Yurie MaedaLaboratory of Cellular and Molecular Neurobiology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan;
Toshihide YamashitaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan; and.
Yoshio HataDivision of Integrative Bioscience, Institute of Regenerative Medicine and Biofunction, Tottori University Graduate School of Medical Sciences, 86 Nishicho, Yonago 683-8503, Japan;
Kazuhiro KitadaDepartment of Biological Sciences, Graduate School of Science, Hokkaido University, Kita-ku, Sapporo 060-0810, Japan.
Nobuhiko YamamotoLaboratory of Cellular and Molecular Neurobiology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan; nobuhiko@fbs.osaka-u.ac.jp.
Osaka University · JPTottori University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axon branching is remodeled by sensory-evoked and spontaneous neuronal activity. However, the underlying molecular mechanism is largely unknown. Here, we demonstrate that the netrin family member netrin-4 (NTN4) contributes to activity-dependent thalamocortical (TC) axon branching. In the postnatal developmental stages of rodents, ntn4 expression was abundant in and around the TC recipient layers of sensory cortices. Neuronal activity dramatically altered the ntn4 expression level in the cortex in vitro and in vivo. TC axon branching was promoted by exogenous NTN4 and suppressed by depletion of the endogenous protein. Moreover, unc-5 homolog B (Unc5B), which strongly bound to NTN4, was expressed in the sensory thalamus, and knockdown of Unc5B in thalamic cells markedly reduced TC axon branching. These results suggest that NTN4 acts as a positive regulator for TC axon branching through activity-dependent expression.

Indexed as

AnimalsAxonsCerebral CortexCoculture TechniquesElectroporationGene Expression ProfilingGene Expression RegulationHEK293 CellsHeterozygoteHumansMiceMice, KnockoutNerve Growth FactorsNetrin ReceptorsNetrinsRatsNerve Growth FactorsNetrin ReceptorsNetrinsNTN4 protein, humanNtn4 protein, mouseReceptors, Cell SurfaceUNC5B protein, humanaxon guidancedevelopmentneocortexneuronal wiring

Identifiers

PMID25288737
PMCPMC4210296
OpenAlexW2153462407

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.