Evidence map›Paper›PMID 16998591›Full record

ArticleNeuron glia biology2004

Myelin associated glycoprotein cross-linking triggers its partitioning into lipid rafts, specific signaling events and cytoskeletal rearrangements in oligodendrocytes.

C B Marta, C M Taylor, S Cheng, R H Quarles, R Bansal, S E Pfeiffer

Open access · greenAbstract read
In one paragraph

Article in Neuron glia biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Quaking I controls a unique cytoplasmic pathway that regulates alternative splicing of myelin-associated glycoprotein.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  7. Review
  8. Article
  9. Article
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  11. Article
  12. The inhibition site on myelin-associated glycoprotein is within Ig-domain 5 and is distinct from the sialic acid binding site.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  13. 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

6 authors at 2 institutions in 2 countries.

C B MartaDepartment of Neuroscience, University of Connecticut Medical School, 263 Farmington Avenue, Farmington, CT 06030-3401, USA. Marta@up.uchc.edu
C M Taylor
S Cheng
R H Quarles
R Bansal
S E Pfeiffer
University of Connecticut · USLaboratory of Molecular Genetics · PL

Funding

PROTEOMIC MAPPING OF MYELIN AND ITS MEMBRANE SUBDOMAINSR01NS041078 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI BANSAL, RASHMI · 2000 to 2009
$3.3M
Oligodendrocyte Differentiation and Myelin BiogenesisR01NS010861 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI BANSAL, RASHMI · 1985 to 2007
$2.3M
GLYCOPROTEINS OF MYELIN IN DEVELOPMENT AND DISEASEZ01NS001808 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI QUARLES, RICHARD · 1985 to 2007
$614k
Functional Organization of the Myelin MembraneF31NS045440 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI TAYLOR, CHRISTOPHER M · 2003 to 2003
$18k
GUKHOLDER AT THE NEUROMUSCULAR JUNCTIONF31NS010861 · NINDS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI GRAMATES, SIAN L · 1999 to 2000
$5k
Intramural NIH HHS Z01 NS001808NINDS NIH HHS F31 NS010861NINDS NIH HHS F31 NS045440NINDS NIH HHS R01 NS010861NINDS NIH HHS R01 NS041078
6 · The paper itself

Abstract

Myelin-associated glycoprotein (MAG) has been implicated in inhibition of nerve regeneration in the CNS. This results from interactions between MAG and the Nogo receptor and gangliosides on the apposing axon, which generates intracellular inhibitory signals in the neuron. However, because myelin-axon signaling is bidirectional, we undertook an analysis of potential MAG-activated signaling in oligodendrocytes (OLs). In this study, we show that antibody cross-linking of MAG on the surface of OLs (to mimic axonal binding) leads to the redistribution of MAG into detergent (TX-100)-insoluble complexes, hyperphosphorylation of Fyn, dephosphorylation of serine and threonine residues in specific proteins, including lactate dehydrogenase and the beta subunit of the trimeric G-protein-complex, and cleavage of alpha-fodrin followed by a transient depolymerization of actin. We propose that these changes are part of a signaling cascade in OLs associated with MAG function as a mediator of axon-glial communication which might have implications for the mutual regulation of the formation and stability of axons and myelin.

Identifiers

PMID16998591
PMCPMC1570761
OpenAlexW2102315592

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.