Evidence map›Paper›PMID 25031414›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Progressive disorganization of paranodal junctions and compact myelin due to loss of DCC expression by oligodendrocytes.

Sarah-Jane Bull, Jenea M Bin, Eric Beaumont, Alexandre Boutet, Paul Krimpenfort, Abbas F Sadikot, Timothy E Kennedy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact, top 93% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. The genetic architecture of fibromyalgia across 2.5 million individuals.medRxiv : the preprint server for health sciences · 2025
    Article
  3. Article
  4. Electrical Forces Improve Memory in Old Age.Reviews of physiology, biochemistry and pharmacology · 2025
    Review
  5. Article
  6. Article
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  8. 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

7 authors at 4 institutions in 3 countries.

Sarah-Jane BullDepartment of Neurology and Neurosurgery and.
Jenea M BinDepartment of Neurology and Neurosurgery and.
Eric BeaumontDépartement de Chirurgie, Université de Montréal, Montreal, Quebec, Canada, H3C 3J7, and.ORCID http://orcid.org/0000-0003-2907-7768
Alexandre BoutetCone Laboratory, Montréal Neurological Institute, McGill University, Montréal, Québec, Canada, H3A 2B4.ORCID http://orcid.org/0000-0001-6942-5195
Paul KrimpenfortDepartment of Molecular Genetics, Cancer Genomics Centre, Centre for Biomedical Genetics, Netherlands Cancer Institute, Amsterdam 1066 CX, The Netherlands.
Abbas F SadikotCone Laboratory, Montréal Neurological Institute, McGill University, Montréal, Québec, Canada, H3A 2B4.
Timothy E KennedyDepartment of Neurology and Neurosurgery and timothy.kennedy@mcgill.ca.
Montreal Neurological Institute and Hospital · CAKennedy Center · DKThe Netherlands Cancer Institute · NLUniversité de Montréal · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Paranodal axoglial junctions are critical for maintaining the segregation of axonal domains along myelinated axons; however, the proteins required to organize and maintain this structure are not fully understood. Netrin-1 and its receptor Deleted in Colorectal Cancer (DCC) are proteins enriched at paranodes that are expressed by neurons and oligodendrocytes. To identify the specific function of DCC expressed by oligodendrocytes in vivo, we selectively eliminated DCC from mature myelinating oligodendrocytes using an inducible cre regulated by the proteolipid protein promoter. We demonstrate that DCC deletion results in progressive disruption of the organization of axonal domains, myelin ultrastructure, and myelin protein composition. Conditional DCC knock-out mice develop balance and coordination deficits and exhibit decreased conduction velocity. We conclude that DCC expression by oligodendrocytes is required for the maintenance and stability of myelin in vivo, which is essential for proper signal conduction in the CNS.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAxonsCell CountDCC ReceptorEmbryo, MammalianEstrogen AntagonistsExploratory BehaviorGap JunctionsIntegrasesMiceMice, TransgenicMicroscopy, Electron, TransmissionMyelin Proteolipid ProteinMyelin SheathNeural ConductionCre recombinaseDcc protein, mouseDCC ReceptorEstrogen AntagonistsIntegrasesMyelin Proteolipid ProteinPlp1 protein, mouseReceptors, Cell SurfaceTamoxifenTumor Suppressor ProteinscasprDCCmyelinnetrinoligodendrocyteparanode

Identifiers

PMID25031414
PMCPMC6608320
OpenAlexW2002232189

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.