Evidence map›Paper›PMID 23407966›Full record

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

Adenomatous polyposis coli regulates oligodendroglial development.

Jordan Lang, Yoshiko Maeda, Peter Bannerman, Jie Xu, Makoto Horiuchi, David Pleasure, Fuzheng Guo

Abstract 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 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

69 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. APC in the nervous system.Medical molecular morphology · 2026
    Review
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  12. Daam2 phosphorylation by CK2α negatively regulates Wnt activity during white matter development and injury.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  20. Group I PAKs in myelin formation and repair of the central nervous system: what, when, and how.Biological reviews of the Cambridge Philosophical Society · 2022
    Review

9 more citing papers are in PubMed but not listed here.

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.

Jordan LangInstitute for Pediatric Regenerative Medicine, University of California, Davis, School of Medicine and Shriners Hospital, Sacramento, California 95817, USA.
Yoshiko Maeda
Peter Bannerman
Jie Xu
Makoto Horiuchi
David Pleasure
Fuzheng Guo

Funding

OLIGODENDROGLIAL PROLIFERATION AND DIFFERENTIATIONR01NS025044 · NINDS · UNIVERSITY OF CALIFORNIA DAVIS · PI PLEASURE, DAVID E. · 1987 to 2011
$3.9M
NINDS NIH HHS R01 NS025044
6 · The paper itself

Abstract

The expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oligodendroglial lineage are poorly understood. We found that immunoreactive APC is transiently induced in the oligodendroglial lineage during both normal myelination and remyelination following toxin-induced, genetic, or autoimmune demyelination murine models. Using the Cre/loxP system to conditionally ablate APC from the oligodendroglial lineage, we determined that APC enhances proliferation of oligodendroglial progenitor cells (OPCs) and is essential for oligodendrocyte differentiation in a cell-autonomous manner. Biallelic Apc disruption caused translocation of β-catenin into the nucleus and upregulated β-catenin-mediated Wnt signaling in early postnatal but not adult oligodendroglial lineage cells. The results of conditional ablation of Apc or Ctnnb1 (the gene encoding β-catenin) and of simultaneous conditional ablation of Apc and Ctnnb1 revealed that β-catenin is dispensable for postnatal oligodendroglial differentiation, that Apc one-allele deficiency is not sufficient to dysregulate β-catenin-mediated Wnt signaling in oligodendroglial lineage cells, and that APC regulates oligodendrocyte differentiation through β-catenin-independent, as well as β-catenin-dependent, mechanisms. Gene ontology analysis of microarray data suggested that the β-catenin-independent mechanism involves APC regulation of the cytoskeleton, a result compatible with established APC functions in neural precursors and with our observation that Apc-deleted OPCs develop fewer, shorter processes in vivo. Together, our data support the hypothesis that APC regulates oligodendrocyte differentiation through both β-catenin-dependent and additional β-catenin-independent mechanisms.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsAntibodiesbeta CateninBlotting, WesternCell DifferentiationCell LineageCells, CulturedEstrogen AntagonistsImmunoprecipitationIn Situ HybridizationMiceMice, KnockoutMicroarray AnalysisMicroscopy, ConfocalMyelin-Associated GlycoproteinAdenomatous Polyposis Coli ProteinAntibodiesbeta CateninEstrogen AntagonistsMyelin-Associated GlycoproteinRNARNA, MessengerTamoxifen

Identifiers

PMID23407966
PMCPMC3711764

What OpenQuestion holds

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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.