Evidence map›Paper›PMID 28935671›Full record

ArticleJournal of cell science2017

EFA6 regulates selective polarised transport and axon regeneration from the axon initial segment.

Richard Eva, Hiroaki Koseki, Venkateswarlu Kanamarlapudi, James W Fawcett

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  5. Hyperactive delta isoform of PI3 kinase enables long-distance regeneration of adult rat corticospinal tract.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  6. Article
  7. Genes in Axonal Regeneration.Molecular neurobiology · 2024
    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

4 authors at 2 institutions in 2 countries.

Richard EvaJohn Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 OPY, U.K.ORCID http://orcid.org/0000-0003-0305-0452
Hiroaki KosekiJohn Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 OPY, U.K.
Venkateswarlu KanamarlapudiInstitute of Life Science, College of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, U.K.
James W FawcettJohn Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 OPY, U.K jf108@cam.ac.uk.ORCID http://orcid.org/0000-0002-7990-4568
University of Cambridge · GBSwansea University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C515455/1Biotechnology and Biological Sciences Research Council BB/C515455/2Medical Research Council G0401232Medical Research Council G1000864Medical Research Council MR/R004544/1
6 · The paper itself

Abstract

Central nervous system (CNS) axons lose their intrinsic ability to regenerate upon maturity, whereas peripheral nervous system (PNS) axons do not. A key difference between these neuronal types is their ability to transport integrins into axons. Integrins can mediate PNS regeneration, but are excluded from adult CNS axons along with their Rab11 carriers. We reasoned that exclusion of the contents of Rab11 vesicles including integrins might contribute to the intrinsic inability of CNS neurons to regenerate, and investigated this by performing laser axotomy. We identify a novel regulator of selective axon transport and regeneration, the ARF6 guanine-nucleotide-exchange factor (GEF) EFA6 (also known as PSD). EFA6 exerts its effects from a location within the axon initial segment (AIS). EFA6 does not localise at the AIS in dorsal root ganglion (DRG) axons, and in these neurons, ARF6 activation is counteracted by an ARF GTPase-activating protein (GAP), which is absent from the CNS, ACAP1. Depleting EFA6 from cortical neurons permits endosomal integrin transport and enhances regeneration, whereas overexpressing EFA6 prevents DRG regeneration. Our results demonstrate that ARF6 is an intrinsic regulator of regenerative capacity, implicating EFA6 as a focal molecule linking the AIS, signalling and transport.This article has an associated First Person interview with the first author of the paper.

Indexed as

Amyloid beta-Protein PrecursorAnimalsAxonal TransportAxon Initial SegmentCerebral CortexDendritesEmbryo, MammalianGanglia, SpinalGene Expression Regulation, DevelopmentalGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsIntegrin alpha ChainsMaleMicrotubulesNeuronsPrimary Cell CultureAmyloid beta-Protein PrecursorGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsIntegrin alpha ChainsPsd protein, ratrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsRNA, Small InterferingAxon initial segmentAxon regenerationAxon transportIntegrinNeuronal polarisationRecycling endosome

Identifiers

PMID28935671
PMCPMC5702059
OpenAlexW2953045849

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.